ライフサイエンスコーパス: normoglycemia

1 ase in apoptosis compared with 5 mM glucose (normoglycemia).

2 with healthy periodontium (while maintaining normoglycemia).

3 in modulating alpha cell function to restore normoglycemia.

4 beta-cell hyperplastic response to maintain normoglycemia.

5 ponse is not sufficient to restore sustained normoglycemia.

6 and human islets restored NRG-Akita mice to normoglycemia.

7 66, P<0.0001), predicted death compared with normoglycemia.

8 graft rejection leading to stable, long-term normoglycemia.

9 emia when compared with 3.3% in grafts under normoglycemia.

10 and beta-cell proliferation and maintaining normoglycemia.

11 y surgical-access but this never resulted in normoglycemia.

12 ersible with insulin treatment that achieved normoglycemia.

13 pressure >12 mm Hg plus glucose to maintain normoglycemia.

14 ients required diazoxide therapy to maintain normoglycemia.

15 70% of them maintained a state of long-term normoglycemia.

16 ell reprogramming, leading to restoration of normoglycemia.

17 y remit hyperglycemia and maintain prolonged normoglycemia.

18 nutrition should probably be treated to true normoglycemia.

19 lase I inhibitor provoked these responses in normoglycemia.

20 transduced with a VEGF vector exhibited near normoglycemia.

21 s a more reliable and durable restoration of normoglycemia.

22 d reducing the number of islets required for normoglycemia.

23 inates autoimmunity and permanently restores normoglycemia.

24 animals that are already diabetic, restores normoglycemia.

25 insulin supplementation that did not restore normoglycemia.

26 ulating porcine C-peptide and maintenance of normoglycemia.

27 NP-depleted animals restored body weight and normoglycemia.

28 d with those who needed high AIR to maintain normoglycemia.

29 f 7 in the subcutaneous tissue site achieved normoglycemia.

30 f pancreatic beta-cells, thereby maintaining normoglycemia.

31 s high in obese individuals, even those with normoglycemia.

32 secretion and induce weight loss to preserve normoglycemia.

33 e of producing human insulin and maintaining normoglycemia.

34 ate insulin secretion for the maintenance of normoglycemia.

35 ion and seem to persist even after return to normoglycemia.

36 CVB infection, were transplanted to restore normoglycemia.

37 ent of type 1 diabetes is the maintenance of normoglycemia.

38 uired a small dose of octreotide to maintain normoglycemia.

39 The control group consisted of 15 rats with normoglycemia.

40 in rats with diabetes compared to those with normoglycemia.

41 to be enhanced during palmitate treatment at normoglycemia.

42 e of species-specific strategies to maintain normoglycemia.

43 aII (PKCbetaII) persisted after returning to normoglycemia.

44 imental vicious cycle despite restoration of normoglycemia.

45 at persists even after the additional 6 h of normoglycemia.

46 9 [10.2] years; 48 men and 54 women; 45 with normoglycemia [44.1%], 31 with prediabetes [30.4%], and

47 The patients were studied at normoglycemia (5-6 mmol/L) and hypoglycemia (2.0-2.5 mmo

48 rown in medium with glucose concentration of normoglycemia (5.5 mM).

49 tight glucose control (TGC) to age-adjusted normoglycemia (50-80 mg/dL at age <1 year and 70-100 mg/

50 in rats with diabetes compared to rats with normoglycemia (69% of baseline versus 93%, respectively,

51 tes, we aimed to determine whether long-term normoglycemia achieved by successful simultaneous pancre

52 In mice, more diabetic recipients reached normoglycemia after intraportal islet transplantation wh

53 re treated with insulin infusion to maintain normoglycemia after surgery.

54 d not translate into a faster achievement of normoglycemia after transplantation, which suggests that

55 ncreasing hypoglycemia, achieved 97% in near normoglycemia and 77% in tight glycemic control, and red

56 Long-term nonfasting normoglycemia and adequate glucose clearance (tolerance

57 the regulation of glycogen synthase both in normoglycemia and diabetes.

58 ted with GDNF restored more diabetic mice to normoglycemia and for a longer period after transplantat

59 eased salvage index both among patients with normoglycemia and hyperglycemia.

60 as well as REC and Muller cells cultured in normoglycemia and hyperglycemic conditions, to investiga

61 tion in all three animals and in a return to normoglycemia and insulin independence in two of three b

62 the results of IIT with regard to attaining normoglycemia and insulin independence of type I diabeti

63 These findings demonstrate that despite normoglycemia and insulin independence, recipients of in

64 The reversal of diabetes was defined by normoglycemia and negative urine glucose maintained for

65 cose concentrations below 15 mmol/L restored normoglycemia and normalized C-peptide.

66 Restoration of normoglycemia and normoinsulinemia in ZDF rats with rosi

67 tion of 300 microg of peptide 5 alone led to normoglycemia and permanent islet survival in three of s

68 in nondiabetic patients reliably establishes normoglycemia and phasic insulin secretion and can achie

69 To evaluate the processes that maintain normoglycemia and regulate BCM during pancreatic regener

70 SPK) transplantation is performed to restore normoglycemia and renal function in patients with type 1

71 tation with MATRIGEL can effectively achieve normoglycemia and that this is a simple and reproducible

72 were associated with durable restoration of normoglycemia and the absence of graft inflammation.

73 tic mice resulted in the restoration of near-normoglycemia and the reversal of diabetic symptoms.

74 s and MSCs resulted in significantly earlier normoglycemia and vascularization, improved glucose tole

75 deling in mouse hepatocytes in comparison to normoglycemia and younger age, respectively.

76 tegies directed at maintaining normothermia, normoglycemia, and prevention of anemia may improve outc

77 f intermediary metabolism and maintenance of normoglycemia, and there is great interest in assessing

78 ive PC subjects were restudied after 72 h of normoglycemia ( approximately 100 mg/dl; variable insuli

79 patic artery (HA protocol) to maintain liver normoglycemia as systemic glucose concentrations were sy

80 h factor/fibroblast growth factor-2 achieved normoglycemia at a higher rate (78%) than control animal

81 The success rate for restoration of normoglycemia at week 4 was highest for the recipients r

82 When blood glucose levels return to normoglycemia beta-cell mass expansion stops, and subseq

83 MST1 deficiency completely restored normoglycemia, beta cell function and survival in vitro

84 either intensive insulin therapy (targeting normoglycemia, between 4.4 and 6.1 mmol/L) or convention

85 and infarct size compared with patients with normoglycemia, but the salvage index and infarct size ad

86 The effect of restoration of normoglycemia by a novel sodium-dependent glucose transp

87 y individuals with normal glucose tolerance, normoglycemia can always be maintained by compensatorily

88 Normoglycemia did not alter ACH-3P proliferation at 2.5%

89 Although control rats maintained near normoglycemia during and after exercise, the rats with i

90 ose production (HGP) is required to maintain normoglycemia during fasting.

91 l mass is a critical factor to help maintain normoglycemia during insulin resistance.

92 min(-1)) to achieve and maintain left renal normoglycemia during systemic hypoglycemia.

93 min(-1)) to achieve and maintain left renal normoglycemia during systemic hypoglycemia.

94 Compared with normoglycemia, exposure of HASMCs to hyperglycemia but n

95 Compared with normoglycemia, exposure of human endothelial cells to hy

96 nd glucagon-like peptide-1 despite achieving normoglycemia faster than animals with renal subcapsular

97 and all six of the KC transplants maintained normoglycemia for > 100 days after the preimmunization r

98 dules was sufficient to restore and maintain normoglycemia for 21 days; the same number of free islet

99 perglycemia, while GABA monotherapy restored normoglycemia for a short period.

100 recipients who have successfully maintained normoglycemia for an average of 10 years and up to 22 ye

101 ved Hb-C-containing microcapsules maintained normoglycemia for at least 8 weeks with normal glucose c

102 Microencapsulated API restored normoglycemia for more than 1 year in spontaneously diab

103 days, two of seven Lef-treated rats remained normoglycemia for more than 100 days.

104 al number of islets cultured in NGF attained normoglycemia for more than 120 days, whereas transplant

105 t graft from immune rejection and maintained normoglycemia for more than 80 days in mice with strepto

106 lycemia; and 2) the restoration of sustained normoglycemia for over 2 years in type I diabetic patien

107 uivalents (IEq) of islets achieved sustained normoglycemia for up to 60 days after islet transplantat

108 CTR increased significantly the time in near normoglycemia from 61 to 74%, simultaneously reducing hy

109 efficiency of engraftment, ability to reach normoglycemia, gain in body weight, response to high glu

110 0.001), and greater in hyperglycemia than in normoglycemia groups (0.503 vs 0.285, p = 0.026).

111 dL) and hyperglycemia (> or =140 mg/dL) with normoglycemia (>70 and <140 mg/dL).

112 xposure to hypoxia/hypoglycemia and normoxia/normoglycemia (H/H-N/N).

113 ive insulin therapy designed to produce near-normoglycemia (HbA(1c) 6.6%).

114 eatment with DST and anti-CD154 mAb restored normoglycemia in 12 of 13 (92%) recipients.

115 marginal dose of 400 islets (n = 5) induced normoglycemia in 20%.

116 Anti-CD154 mAb monotherapy restored normoglycemia in 4 of 10 (40%) NPCC-engrafted, chemicall

117 s targeting IKKbeta resulted in reversion to normoglycemia in 50% of streptozotocin-induced diabetic

118 mmune encephalomyelitis, as well as maintain normoglycemia in a mouse model of type 1 diabetes.

119 rce of local immunosuppression would lead to normoglycemia in a streptozotocin-induced diabetic mouse

120 ulated glucagon release sufficient to attain normoglycemia in both diabetic and prediabetic stages.

121 ze after coronary artery occlusion, prolongs normoglycemia in diabetic mice after pancreatic islet tr

122 pancreatic islet-like structures and support normoglycemia in diabetic mice.

123 erior to anti-CD20 monotherapy for restoring normoglycemia in diabetic NOD mice, providing important

124 transplantation aims to restore physiologic normoglycemia in diabetic patients with glomerulopathy a

125 d as a powerful clinical modality to restore normoglycemia in diabetic patients.

126 s, graft sizes of 700 or 500 islets restored normoglycemia in eight of nine or five of eight animals,

127 NPCC fully differentiated and restored normoglycemia in four of five diabetic NOD-scid recipien

128 al opinion collated, and the Web site of the Normoglycemia in Intensive Care Evaluation and Survival

129 ecently completed large international study, Normoglycemia in Intensive Care Evaluation and Survival

130 cemia in NIDDM and may prevent attainment of normoglycemia in most patients who are using the convent

131 tigen-based therapies (ABTs) fail to restore normoglycemia in newly diabetic NOD mice, perhaps becaus

132 ta-cell replication, and effectively restore normoglycemia in newly diabetic NOD mice.

133 reversible, impaired glucose tolerance with normoglycemia in pancreatic beta cells; wound healing an

134 ctional beta cells, which may help restoring normoglycemia in patients suffering from diabetes.

135 ortant goal for therapies aimed at restoring normoglycemia in patients with diabetes.

136 Restoration of normoglycemia in patients with long-standing T1D via kid

137 roven to be a successful strategy to restore normoglycemia in patients with type 1 diabetes (T1D).

138 n acceptable clinical modality for restoring normoglycemia in patients with type 1 diabetes mellitus

139 sive therapy with insulin, which establishes normoglycemia in rats with diabetes, prevents the delay

140 rved functional beta-cell mass, and restored normoglycemia in recent-onset NOD mice, even when hyperg

141 ogic responses to secretagogues and restored normoglycemia in streptozotocin-induced diabetic severe

142 an encapsulation strategy to establish near-normoglycemia in subjects with T1D, assuming that glucos

143 Patient and pancreas (normoglycemia in the absence of any antidiabetic therapy

144 ion: insulin secretion increases to maintain normoglycemia in the face of insulin resistance and/or d

145 Combined treatment restored normoglycemia in the long term with apparent permanent r

146 Even though it is possible to achieve normoglycemia in the majority of recipients by this meth

147 pigs, these were not sufficient to maintain normoglycemia in the monkeys.

148 ting insulin enable the LID mice to maintain normoglycemia in the presence of apparent insulin insens

149 ve mechanism that enables the maintenance of normoglycemia in the presence of insulin resistance.

150 ppear essential for permanent restoration of normoglycemia in this T1DM model.

151 the full differentiation state and restoring normoglycemia in transgenic mice.

152 inhibitor, prolongs islet graft survival and normoglycemia in transplanted allogeneic diabetic mice,

153 n acceptable clinical modality for restoring normoglycemia in type 1 diabetic patients, there is a cr

154 pression has been shown to result in fasting normoglycemia in type 1 diabetic rats, although the trea

155 Recovery with normoglycemia is accompanied by a significant improvemen

156 In many organisms, normoglycemia is achieved by a tight coupling of nutrien

157 In comparison to studies suggesting that normoglycemia is an easily achievable goal, our protocol

158 ng daily blood glucose (diabetes >300 mg/dL, normoglycemia <150 mg/dL).

159 POI by 30% with every 40-point increase from normoglycemia (<110 mg/dL).

160 ion, all recipients developed and maintained normoglycemia (<120 mg/dl) and stable renal function ind

161 and 3 achieved sustained insulin-independent normoglycemia (median rejection-free survivals 60 and 11

162 to its usual inflammatory function, restores normoglycemia, most likely by localized bystander suppre

163 l dose islet transplant with nIgM to restore normoglycemia (n = 4).

164 n = 2), 11.1% in the obese participants with normoglycemia (n = 5), 29% in the obese participants wit

165 mice with nIgM (75 mug 3x per week) restored normoglycemia (n = 5), whereas severely diabetic mice re

166 erived insulin contributed to restoration of normoglycemia, near-total pancreatectomy resulted in hyp

167 ine aortic endothelial cells were exposed to normoglycemia (NG, 5.0 mM) or hyperglycemia (30 mM).

168 signed to truly optimize control within near normoglycemia of 3.9-10 mmol/L.

169 Based on the stable normoglycemia of mice with type 1 diabetes during suppre

170 nduced hypoglycemia was obtained by reaching normoglycemia or hyperglycemia for another 2 h and then

171 cultured retinal endothelial cells (REC) in normoglycemia or hyperglycemia to determine the interact

172 Medical record data from newborns with normoglycemia or transient hypoglycemia were matched wit

173 ulin sensitivity and lipids in patients with normoglycemia or type 2 diabetes.

174 ced fasting blood insulin levels, maintained normoglycemia over a 24-hour fast, and had no evidence o

175 rom WT to IL-18BP-Tg mice achieved prolonged normoglycemia (P = 0.031).

176 Normoglycemia persisted 10-80 days without other treatme

177 etransduced with Ang-1 vector exhibited near normoglycemia posttransplantation.

178 I diabetic patients and consequent long-term normoglycemia reestablishes native alpha-cell responses

179 mass, islets purified by filtration restored normoglycemia significantly faster than those isolated b

180 All three animals maintained normoglycemia thereafter.

181 that mice can survive sepsis by maintaining normoglycemia through ferritin's capacity to inactivate

182 e the number of recipients who could achieve normoglycemia through islet transplantation if the curre

183 unctional microorgan involved in maintaining normoglycemia through regulated secretion of insulin and

184 The transition of an individual from normoglycemia to diabetes has generally been thought to

185 Islet transplantation can restore normoglycemia to patients with unstable type 1 diabetes

186 ate blood levels ranging from 5.9 +/- 1.8mM (normoglycemia) to 21 +/- 2.3mM.

187 rance) and -6 g/L (95% CI: -8.47, -3.53 g/L; normoglycemia)], triglycerides (-0.08 mmol/L; 95% CI: -0

188 with basal hepatic insulin production, near-normoglycemia under both fed and fasting conditions was

189 a milder phenotype that is characterized by normoglycemia, unless the animals are stressed.

190 xperiments, all of the rats (n=4) maintained normoglycemia up to 210 days after transplantation.

191 ent hyperglycemia, VLBW infants can maintain normoglycemia via gluconeogenesis from glycerol and amin

192 smallest graft size to consistently restore normoglycemia was 1,000 islets.

193 eic transplantation, time taken to return to normoglycemia was 15.4 +/- 3.6 days for nIgM-treated rec

194 cemia in transplanted mice within 1 week and normoglycemia was achieved after 5 weeks.

195 In allografts, after normoglycemia was achieved and stable luminescence inten

196 Normoglycemia was achieved at the same rate in both grou

197 Although normoglycemia was achieved earlier with tight glycemic c

198 Normoglycemia was achieved in all three groups 14 days a

199 Normoglycemia was achieved in only 1/7 mice receiving rA

200 Transient normoglycemia was achieved in treated mice two days afte

201 without the need for insulin injections, and normoglycemia was attained within 2 weeks.

202 Restoration of normoglycemia was attributable to an enhancement in key

203 ection may also occur in the hepatic artery, normoglycemia was established across the liver via a loc

204 However, when 40,000 IEQ/kg were infused, normoglycemia was lost within five days, but when 80,000

205 When portohepatic normoglycemia was maintained during POR(UPS), a 67% supp

206 conclude that in VLBW infants receiving TPN, normoglycemia was maintained during reduced glucose infu

207 reatic islet function to such an extent that normoglycemia was maintained in up to 75% of animals aft

208 after the pancreatectomy, and in both cases normoglycemia was maintained thereafter by the TIK.

209 t grafts, despite a marginal islet dose, and normoglycemia was maintained until graft explantation.

210 in-load dependent (r = 0.83, P < 0.001), and normoglycemia was maintained.

211 when 80,000 IEQ/kg were infused in one case, normoglycemia was more persistent.

212 Normoglycemia was not achieved with 1200 islets in the u

213 ion model, the median time needed to achieve normoglycemia was reduced from 17.0 days among untreated

214 The attainability of posttransplantation normoglycemia was significantly higher in the 4 degrees

215 The proportion of mice that achieved normoglycemia was significantly higher in the group impl

216 mal within 1 week after transplantation, and normoglycemia was sustained for at least 6 weeks without

217 ltration and beta-cell division and restored normoglycemia when given to hyperglycemic mice at the pr

218 erior to wild-type donor islets in achieving normoglycemia when transplanted into KO diabetic recipie

219 ent was associated with prompt and sustained normoglycemia, whereas the untreated islet graft recipie

220 valents in GFS-VEGF+HGF were able to restore normoglycemia, whereas those transplanted in GFR failed

221 so appears that perioperative maintenance of normoglycemia will become a valid performance measure fo

222 nctionality in vivo: recipient mice achieved normoglycemia with a comparable tempo, whereas loss of g

223 Subjects who maintained normoglycemia with a low AIR had an increased proinsulin

224 , but they exhibited a more durable state of normoglycemia with greater insulin reserves.

225 Islet cell transplantation resulted in normoglycemia within 24 hr.

226 ransplantation into the scaffold resulted in normoglycemia within 3 days and for the duration of the

227 vels in both models, and all animals reached normoglycemia within the first days after transplantatio

228 At term equivalent age, normoglycemia without any insulin treatment was found in

229 ix portal vein experiments, animals achieved normoglycemia without exogenous insulin.