ライフサイエンスコーパス: diabetic animal

1 > 600 nmol/mg mito prot, in both control and diabetic animals.

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

3 ace epithelium observed in poorly controlled diabetic animals.

4 hosphorylation was observed in the retina of diabetic animals.

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

6 not decrease lesion volume in insulinopenic diabetic animals.

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

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

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

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

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

12 ulointerstitial compartments of experimental diabetic animals.

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

14 tochemistry in healing craniotomy defects in diabetic animals.

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

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

17 evelopment of renal and retinal pathology in diabetic animals.

18 alent modification were found in aortae from diabetic animals.

19 n the glomerular and tubular compartments of diabetic animals.

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

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

22 epinephrine response to hypoglycemia in STZ-diabetic animals.

23 tions that G6Pase expression is increased in diabetic animals.

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

25 n pancreas sections compared with those from diabetic animals.

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

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

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

29 r abnormal retinal and renal hemodynamics in diabetic animals.

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

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

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

33 and distal ends was significantly reduced in diabetic animals.

34 ssure-induced constrictions of arteries from diabetic animals.

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

36 location and reduced blood glucose levels in diabetic animals.

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

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

39 vels were higher in cerebral microvessels of diabetic animals.

40 s were increased significantly vs. untreated diabetic animals.

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

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

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

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

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

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

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

48 pecific fatty acid metabolism in control and diabetic animals.

49 actions results in severe renal pathology in diabetic animals.

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

51 gnalling may contribute to hyperglycaemia in diabetic animals.

52 appaB p50 expression compared with untreated diabetic animals.

53 ered mitochondrial function in the hearts of diabetic animals.

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

55 r dysfunction and improve stroke recovery in diabetic animals.

56 d LV function were significantly impaired in diabetic animals.

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

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

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

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

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

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

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

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

65 Diabetic animals also demonstrated reduced endothelial c

66 The diabetic animals also had significantly elevated VEGF pr

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

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

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

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

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

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

73 All diabetic animals and approximately 20% of nondiabetic an

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

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

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

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

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

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

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

81 Diabetic animals and nondiabetic controls were monitored

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 In diabetic animals, delayed gastric emptying can be revers

106 Isolated ventricular myocytes from diabetic animals demonstrate impaired relaxation concomi

107 Diabetic animals demonstrated a significantly reduced bo

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

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

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

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

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

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

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

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

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

117 Neutrophils from diabetic animals exhibit higher levels of surface integr

118 Diabetic animals exhibited increased vascular expression

119 Diabetic animals exhibited significant endothelial dysfu

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

121 Diabetic animals fed on a HFD showed an increased upregu

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

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

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

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

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

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

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

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

130 In diabetic animals, immunohistochemistry and Western blott

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

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

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

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

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

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

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

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

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

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

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

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

143 9 treatment restored the loss of glycogen in diabetic animals lacking insulin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 In diabetic animal models, hyperglycemia results in hyperco

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

164 sfunction and morphological abnormalities in diabetic animal models.

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

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

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

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

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

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

171 ncrease insulin sensitivity in two different diabetic animal models.

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

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

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

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

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

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

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

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

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

181 1 expression were ameliorated in DOX-treated diabetic animals (P < 0.05).

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

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

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

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

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

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

188 Diabetic animals receiving a marginal mass of 300 islets

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

190 Diabetic animals receiving doxycycline did not differ si

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

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

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

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

195 Diabetic animals showed a small but significant delay in

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

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

198 Diabetic animals showed significantly higher blood gluco

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

200 In diabetic animals, significantly impaired peripheral opio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

220 The diabetic animals underwent DJB or sham surgery.

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

222 1b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expre

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

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

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

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

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

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

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

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

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

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

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

234 Confirmed diabetic animals were treated with a highly specific VEG

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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