ライフサイエンスコーパス: diabetic animal

1 ered mitochondrial function in the hearts of diabetic animals.

2 ased specific activity of GAPDH in muscle of diabetic animals.

3 d LV function were significantly impaired in diabetic animals.

4 , more strongly for healthy animals than for diabetic animals.

5 expression of TSP-1 in the large arteries of diabetic animals.

6 reduced myelin content in the cortex of the diabetic animals.

7 he podocyte membrane to the cytoplasm in the diabetic animals.

8 ace epithelium observed in poorly controlled diabetic animals.

9 hosphorylation was observed in the retina of diabetic animals.

10 icantly increased in the liver and kidney of diabetic animals.

11 not decrease lesion volume in insulinopenic diabetic animals.

12 ss of albumin led to hypoalbuminemia in some diabetic animals.

13 time and this stability was not disturbed in diabetic animals.

14 aring levels of GALP mRNA between normal and diabetic animals.

15 ic value and rate of decay) in myocytes from diabetic animals.

16 ulointerstitial compartments of experimental diabetic animals.

17 od-retinal barrier breakdown worsened in the diabetic animals.

18 tochemistry in healing craniotomy defects in diabetic animals.

19 ts, with levels remaining elevated longer in diabetic animals.

20 ted nitric oxide increases in the retinae of diabetic animals.

21 > 600 nmol/mg mito prot, in both control and diabetic animals.

22 evelopment of renal and retinal pathology in diabetic animals.

23 alent modification were found in aortae from diabetic animals.

24 n the glomerular and tubular compartments of diabetic animals.

25 ks or 3 days) for established streptozotocin-diabetic animals.

26 ased retinal blood flow (RBF) in control and diabetic animals.

27 tions that G6Pase expression is increased in diabetic animals.

28 old from 5:1 in control rats to 0.2:1 in the diabetic animals.

29 n pancreas sections compared with those from diabetic animals.

30 of diabetic mothers and in the offspring of diabetic animals.

31 se by liver and kidney are both increased in diabetic animals.

32 fasted animals and 3-8-fold in the livers of diabetic animals.

33 r abnormal retinal and renal hemodynamics in diabetic animals.

34 raft rejection in streptozocin (STZ)-induced diabetic animals.

35 d the response to pinacidil in arteries from diabetic animals.

36 and distal ends was significantly reduced in diabetic animals.

37 ssure-induced constrictions of arteries from diabetic animals.

38 s similar to those observed in arteries from diabetic animals.

39 n to inhibit renal and vascular pathology in diabetic animals.

40 gnalling may contribute to hyperglycaemia in diabetic animals.

41 alpha-MD) were 2-10-fold lower in tissues of diabetic animals.

42 r dysfunction and improve stroke recovery in diabetic animals.

43 itro and to mediate oral Insulin activity in diabetic animals.

44 d type 2 diabetes, even in insulin-deficient diabetic animals.

45 une suppression and induces normoglycemia in diabetic animals.

46 did LECs and migrated cells in the lenses of diabetic animals.

47 ocyte (Mono) trafficking into the retinas of diabetic animals.

48 epinephrine response to hypoglycemia in STZ-diabetic animals.

49 n compared with that in normal or moderately diabetic animals.

50 tures from fundus images of diabetic and non-diabetic animals.

51 location and reduced blood glucose levels in diabetic animals.

52 vels were higher in cerebral microvessels of diabetic animals.

53 s were increased significantly vs. untreated diabetic animals.

54 of donor cells derived from both healthy and diabetic animals.

55 ailability, was enhanced in the podocytes of diabetic animals.

56 explain how TIE2 signaling is attenuated in diabetic animals.

57 the primary renal cells and in the kidney of diabetic animals.

58 ber of degenerate (acellular) capillaries in diabetic animals.

59 and survivin, 4 days after treatment in the diabetic animals.

60 ) in many cell types and in kidney tissue of diabetic animals.

61 ing activity of nuclear factor-kappaB in the diabetic animals.

62 pecific fatty acid metabolism in control and diabetic animals.

63 actions results in severe renal pathology in diabetic animals.

64 enzymes involved in fat oxidation in type 2 diabetic animals.

65 appaB p50 expression compared with untreated diabetic animals.

66 In preclinical diabetic animals, 19 was found to robustly lower fasting

67 cytosol and 24% was particulate, whereas in diabetic animals, 55% was cytosolic and 45% was particul

68 l/L) was significantly less in arteries from diabetic animals (68+/-5%) than in normal vessels (90+/-

69 n of RyR2 from 8-week streptozotocin-induced diabetic animals (8D) afforded 21% fewer peptides, where

70 In diabetic animals, acute blockade of O-GlcNAc inhibited a

71 her within the livers, kidneys, and lungs of diabetic animals administered the anti-DMPO probe compar

72 Diabetic animals also demonstrated reduced endothelial c

73 The diabetic animals also had significantly elevated VEGF pr

74 TNF inhibition in diabetic animals also reduced apoptosis, increased proli

75 In diabetic animals, ALT-711 improved left ventricular func

76 ivated preferentially in the vasculatures of diabetic animals, although other PKC isoforms are also i

77 r increase in osteopontin mRNA expression in diabetic animals, amounting to 570 +/- 73% (mean +/- SE,

78 In diabetic animals an agonist (epibatidine, 10(-10) mol/L)

79 m were 1.4 and 0.6 mumol/L, respectively, in diabetic animals and 0.3 and 0.04, respectively, in cont

80 All diabetic animals and approximately 20% of nondiabetic an

81 changes similar to those observed in T2D and diabetic animals and has profound effects on insulin sec

82 ated myofibril has been described in chronic diabetic animals and humans.

83 muscle, and adipose tissues in obese and/or diabetic animals and in obese human patients.

84 kidney cortical tissue of control and type 1 diabetic animals and in proximal tubular cells incubated

85 dothelin-1 was also increased in 12-week-old diabetic animals and in those maintained on insulin thro

86 y, is specifically increased in the heart of diabetic animals and is regulated by hyperglycemia and i

87 te antibodies, analyses of kidney lysates of diabetic animals and LLC-PK1/HK-2 cells subjected to HG

88 flow in the retina and peripheral nerves of diabetic animals and may be related to the development o

89 Diabetic animals and nondiabetic controls were monitored

90 ates, commonly observed in the myocardium of diabetic animals and patients, are postulated to contrib

91 recede clinical diabetic retinopathy in both diabetic animals and patients.

92 a proven strategy for decreasing glucose in diabetic animals and patients.

93 tein and mRNA are substantially decreased in diabetic animals and rapidly restored by the administrat

94 re elevated in insulin-responsive tissues of diabetic animals and that agents which trigger ceramide

95 albumin-derived urinary peptide excretion in diabetic animals, and hyperglycemia modulated this pepti

96 ments, we excised the aorta from control and diabetic animals, and measured TLR4 and MD2-a co-recepto

97 inal function reproducibly detected in these diabetic animals, and Nepafenac significantly inhibited

98 ), and NADPH levels were markedly reduced in diabetic animals, and PARP-inhibitor treatment was able

99 ow decreases comparable to those measured in diabetic animals, and the subsequent injection of 10(-4)

100 abetes-accelerated atherosclerosis, in which diabetic animals are hyperglycemic without receiving exo

101 , and the cell size reduced in the cortex of diabetic animals as assessed by DNA/wet weight of brain

102 normal animals and promotes wound healing in diabetic animals as well as growth factors, yet neither

103 and 31%, respectively) compared to untreated diabetic animals as well as in normal rats (29%).

104 eactive RKBP were significantly lower in the diabetic animals at each time point examined compared to

105 dysfunction and facilitates wound healing in diabetic animals, at least partly through preventing MGO

106 showed VEGFR-2 expression in capillaries of diabetic animals but not in normal controls.

107 ffect on vitreal glutamate concentrations in diabetic animals but significantly decreased vitreoretin

108 nce was blunted in delayed healing wounds of diabetic animals but, topical tissue nanotransfection of

109 lialization and accelerates wound closure in diabetic animals by targeting epithelial sodium channels

110 ion in the retina and retinal capillaries of diabetic animals cannot be attributed to fewer vessels.

111 The survival time of diabetic animals chronically treated with oral insulin +

112 tion velocity was significantly decreased in diabetic animals compared to controls.

113 th delays ranging from 11% to 17-fold in the diabetic animals compared with control counterparts.

114 mulation of PGC-GdDTPA-F in the pancreata of diabetic animals compared with controls.

115 assessed by echocardiography in the treated diabetic animals compared with the nontreated diabetic c

116 elevated retrograde axonal transport in STZ-diabetic animals (control 1.0 +/- 0.07, diabetic 3.0 +/-

117 In diabetic animals, delayed gastric emptying can be revers

118 Isolated ventricular myocytes from diabetic animals demonstrate impaired relaxation concomi

119 Diabetic animals demonstrated a significantly reduced bo

120 In vivo, diabetic animals demonstrated an impaired ability to inc

121 in-Alexa568 and 69-kD FITC-dextran; however, diabetic animals demonstrated significantly less filtere

122 difference in solubility between normal and diabetic animals demonstrated that Charles River animals

123 The density of capillaries in retinas of diabetic animals did not change from normal, and so the

124 Hearts from type 2 diabetic animals display perturbations in excitation-con

125 tigated whether LTCC function is affected in diabetic animals due to reduced PI 3-kinase signaling.

126 icular SVs were significantly altered in all diabetic animals; EDVs and EFs significantly altered in

127 been used to study catecholamine turnover in diabetic animals, effects of diabetes on metabolism of t

128 on of T cells with a Tfh cell phenotype from diabetic animals efficiently transferred diabetes to rec

129 In diabetic animals, elevated ER stress markers, ATF4, and

130 Neutrophils from diabetic animals exhibit higher levels of surface integr

131 Diabetic animals exhibited increased vascular expression

132 Diabetic animals exhibited significant endothelial dysfu

133 We show that diabetic animals fed a cholesterol-rich diet, like human

134 Diabetic animals fed on a HFD showed an increased upregu

135 , RAGE, TNF-alpha, VEGF and 5-LO was seen in diabetic animals fed on HFD compared to the other groups

136 strated that infarct volumes were greater in diabetic animals following middle cerebral artery occlus

137 nes induced by the rexinoids and the TZDs in diabetic animals found in these studies suggests that th

138 Aminoguanidine-treated diabetic animals had a significantly greater MBIC than t

139 n contrast, grafts placed in insulin-treated diabetic animals had increased numbers of mesangial cell

140 t assays revealed that nuclear extracts from diabetic animals had reduced binding to the MEF2 binding

141 hat both insulinopenic and insulin-resistant diabetic animals have increased apoptosis in the CNS in

142 results indicated that craniotomy defects in diabetic animals healed approximately 40% of the degree

143 In diabetic animals, immunohistochemistry and Western blott

144 Maintaining diabetic animals in a dim-adapting light did not slow th

145 the a- and b-wave properties of the ERGs of diabetic animals in parallel with the changes in oscilla

146 dow of solubility between the normal and the diabetic animals in the former.

147 ity in vitro and retinal vascular leakage in diabetic animals in vivo.

148 n the retina and allodynia were inhibited in diabetic animals in which iNOS or PARP1 was deleted from

149 ificantly lower number of pericytes than non-diabetic animals.Increased retinal immunoreactivity of G

150 nalysis of vessels from insulin resistant or diabetic animals indicates that CREB content is decrease

151 In addition, transfer of CD8(+) T cells from diabetic animals into DORmO.RAG2(-/-) mice promoted insu

152 of MSCs in the liver and skeletal muscles in diabetic animals is also enhanced and therefore improves

153 The impairment in tissue repair in diabetic animals is at least partially due to a deficien

154 ve beta-cells (A+) following pair-feeding of diabetic animals is due to beta-cell restoration.

155 data revealed that the rate of digestion for diabetic animals is markedly slow relative to that of no

156 ion and bacterial proliferation increased in diabetic animals: isoproterenol stimulated SGLT1 migrati

157 inetics relationship does not change form in diabetic animals; it is merely shifted (delayed) on the

158 9 treatment restored the loss of glycogen in diabetic animals lacking insulin.

159 ed Ca(2+) permeability of these receptors in diabetic animals leads to reduced release of GABA, follo

160 uggest that increased polyol pathway flux in diabetic animals leads to the activation of p38.

161 cant increase in plasma leptin levels in the diabetic animals maintained on the HF, and large differe

162 ion of either G(L) or G(M)/R(Gl) in liver of diabetic animals may represent a strategy for lowering o

163 data suggest that mechanical hyperalgesia in diabetic animals may, at least in part, result from foca

164 g inflammatory cytokines and chemokines in a diabetic animal model while improving fasting glucose le

165 hite adipose tissue is downregulated in this diabetic animal model, and that PDE3A and PDE3B genes ar

166 Lepr(db/db) mice, an obese/diabetic animal model, exhibit reduced Sirt6 levels; ect

167 In a pancreatectomised diabetic animal model, exogenous Pref-1 improved glucose

168 stations of diabetic nephropathy in a type 1 diabetic animal model, OVE26.

169 Using a type 1 diabetic animal model, TCS potentiates and accelerates t

170 In the diabetic animal model, the duration of action of [N(epsi

171 thophysiological consequences in this type 2 diabetic animal model.

172 gnaling and improve insulin sensitivity in a diabetic animal model.

173 g dramatic glucose lowering in ob/ob mice, a diabetic animal model.

174 poRon (APR) in experimental periodontitis in diabetic animal models and demonstrated the underlying m

175 ulin resistance and hyperinsulinemia in both diabetic animal models and NIDDM subjects.

176 ulin resistance and hyperinsulinemia in both diabetic animal models and NIDDM subjects.

177 nase 5 (Erk5) is lost in the hearts of obese/diabetic animal models and that cardiac-specific deletio

178 nd the therapeutic effects of PM observed in diabetic animal models depend, at least in part, on its

179 art of diabetic patients and in experimental diabetic animal models have been reported.

180 Recent studies in diabetic animal models identify decreased cardiomyocyte

181 In diabetic animal models, hyperglycemia results in hyperco

182 In diabetic animal models, the administration of recombinan

183 ncrease insulin sensitivity in two different diabetic animal models.

184 nse to stent injury in insulin-resistant and diabetic animal models.

185 sfunction and morphological abnormalities in diabetic animal models.

186 rity-onset diabetes of the young and in some diabetic animal models.

187 inhibitors, however, do not lower glucose in diabetic animal models.

188 both insulin-deficient and insulin-resistant diabetic animal models.

189 tasis both in vitro and in vivo in different diabetic animal models.

190 s latent TGF-beta activation in vitro and in diabetic animal models.

191 cy in lowering glucose levels in preclinical diabetic animal models.

192 ted using a variety of rodent cell lines and diabetic animal models.

193 tinal Evans blue leakage of eyes from 1-week diabetic animals (n = 11 retinas) was 1.7-fold higher (P

194 In the diabetic animals, NET mRNA was significantly elevated (1

195 In diabetic animals, neutralizing antibodies targeting seru

196 nd islet grafts were performed in chemically diabetic animals, no adverse effect of either clinical o

197 resistant to BQ-123, the maximal response in diabetic animals occurred 20 minutes later than in nondi

198 increased in glomeruli or renal cortex from diabetic animals or in mesangial cells cultured in high

199 did not differ significantly from untreated diabetic animals (P > 0.05).

200 1 expression were ameliorated in DOX-treated diabetic animals (P < 0.05).

201 nched chain AA valine, which was elevated in diabetic animals (P < 0.05).

202 compared with the wound-healing rate in non-diabetic animals (P < 0.05).

203 r by dobutamine was significantly blunted in diabetic animals (p < 0.05).

204 VEGFR-2) in retinal and choroidal vessels of diabetic animals (P<0.01), compared to normal controls.

205 f blood flow especially in the insulinopenic diabetic animals paradoxically exacerbates this process.

206 actosemia, and administration of LY333531 to diabetic animals prevented these abnormalities.

207 transcription factor, which is repressed in diabetic animals, promotes vascular endothelial cell (EC

208 In the retinas of diabetic animals, protein kinase C (PKC) activity is ele

209 d the development of diabetic retinopathy in diabetic animals, raising the possibility that anti-infl

210 ved the function of transplanted islets with diabetic animals rapidly re-establishing glycemic contro

211 Diabetic animals receiving a marginal mass of 300 islets

212 cative of leukostasis, were only observed in diabetic animals receiving control AAV injections.

213 Diabetic animals receiving doxycycline did not differ si

214 sterol intake by the control and STZ-induced diabetic animals reduced plasma cholesterol levels in ST

215 d in cardiocytes isolated from the hearts of diabetic animals relative to control animals (P < .01).

216 ion of exogenous 14S,21R-diHDHA to wounds in diabetic animals rescued healing and angiogenesis.

217 nsulin-deficient streptozotocin (STZ) or NOD diabetic animals, resulted in near normalization of gluc

218 formatic interrogation of the acetylome from diabetic animals showed a predominance of metabolic path

219 Diabetic animals showed a small but significant delay in

220 Dorsal root ganglia (DRG) from diabetic animals showed marked activation of p38 at 12 w

221 In contrast, diabetic animals showed significant differences in the p

222 Diabetic animals showed significantly higher blood gluco

223 Both intravitreally CXCL1-injected and diabetic animals showed significantly increased retinal

224 More strikingly, the kinetics of the diabetic animals showed the feature of a lag in digestio

225 In diabetic animals, significantly impaired peripheral opio

226 Our results demonstrate that in diabetic animal strains repetitive ambient ozone exposur

227 Different from nondiabetic mice, diabetic animals submitted to mild sepsis displayed a si

228 oroidal blood flow was reduced even in young diabetic animals, suggesting ocular blood flow deficit c

229 tic reduction of podocyte-specific mTORC1 in diabetic animals suppressed the development of DN.

230 he hypothalamus, medulla/pons, and plasma of diabetic animals than in controls.

231 ndetectable at the BBM of control animals or diabetic animals that had been fasted overnight.

232 Ocular ET-1 levels were elevated twofold in diabetic animals that received insulin treatment for 7 d

233 At 4 and 8 weeks, diabetic animals that were receiving NTX had an accelera

234 eration in reepithelialization compared with diabetic animals that were receiving vehicle and even su

235 d the labeling index by up to eightfold from diabetic animals that were receiving vehicle.

236 lockade of the TLR4-MD2 complex lowers BP in diabetic animals; that (b) type 1 diabetes modulates the

237 Moreover, in diabetic animals, the increased pathogenicity could be s

238 In neurons from diabetic animals, the opiate agonist dynorphin A (Dyn A;

239 ed together with 14S,21R-diHDHA to wounds in diabetic animals, they coacted to accelerate wound re-ep

240 lthough plasma GLP-1 levels were elevated in diabetic animals, this was accompanied by increased rath

241 toxicity, inflammation, and BRB breakdown in diabetic animals through activities that may involve inh

242 osed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phospho

243 eptozotocin-induced diabetic Lewis rats, and diabetic animals treated with aminoguanidine and two nov

244 Glucose tolerance tests comparing diabetic animals treated with porcine islet macrobead im

245 Diabetic animals treated with prodrugs, once daily for 5

246 Blood-retinal barrier breakdown in diabetic animals treated with solvent alone or IL6R Trap

247 endothelial growth factor in nondiabetic and diabetic animals treated with tin protoporphyrin (SnPP,

248 levels are decreased in both lean and obese diabetic animals treated with TZDs.

249 The diabetic animals underwent DJB or sham surgery.

250 e wound strengthening was more pronounced in diabetic animals using a CMV-driven construct.

251 1b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expre

252 arly, retinal vascular permeability in 8-day diabetic animals was 1.8-fold higher than in normal nond

253 Significantly delayed wound closure in diabetic animals was associated with diminished circulat

254 n distribution and in TnI phosphorylation in diabetic animals was completely prevented by rendering t

255 Pancreatic uptake in diabetic animals was decreased by more than 80% (P < 0.0

256 generation by intact isolated glomeruli from diabetic animals was increased compared with glomeruli i

257 defective counterregulatory response in STZ-diabetic animals was restored to normal with either loca

258 The retinal vascular endothelium of the diabetic animals was stained for ADPase activity in flat

259 Retinal VEGF mRNA levels in 1-week diabetic animals were 3.2-fold higher than in nondiabeti

260 Moreover, oocytes from diabetic animals were exquisitely sensitive to NOS and g

261 ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabe

262 aicin and elevated KCl recorded in DRGs from diabetic animals were significantly larger than those re

263 Confirmed diabetic animals were treated with a highly specific VEG

264 ine the role of insulin in vivo, STZ-induced diabetic animals were treated with background insulin an

265 Some groups of normal and diabetic animals were treated with captopril (10 mg/kg p

266 Diabetic animals were treated with FeTPPS (15 mg x kg(-1

267 Striking enhancements in footprints from diabetic animals were visible at -142 and at -161 (in th

268 terious to vascular function in the maternal diabetic animals when assessed in mesenteric arteries 16

269 Amplitude-matched OPs were delayed in diabetic animals when compared with baseline data from t

270 psulated islets can reverse hyperglycemia in diabetic animals when transplanted i.p. or into the fat

271 cemia, VMH GABA levels did not change in the diabetic animals, whereas they significantly declined in

272 nt reduction in the mean endoneurial area in diabetic animals with 5 and 8 mm gaps compared to contro

273 Treatment of STZ-diabetic animals with 5 mg/kg human recombinant NT-3 pre

274 Treatment of diabetic animals with a specific inhibitor of p38 (SB 23

275 d when coculturing leukocytes from wild-type diabetic animals with retinal endothelium.

276 Treating STZ-induced diabetic animals with the RCS scavenger, pyridoxamine, b

277 We found that diabetic animals with transplanted islets showed a signi

278 and restored corneal surface sensitivity in diabetic animals without causing toxic side effects.

279 and calcium ATPase activities in retinas of diabetic animals without having any beneficial effect on