ライフサイエンスコーパス: hypoglycaemia

1 4 to 0.88; p=0.0131; 25.5%vs 33.6% had minor hypoglycaemia).

2 ts with type 2 diabetes with minimum risk of hypoglycaemia.

3 a role in the counterregulatory response to hypoglycaemia.

4 and was well tolerated with minimum risk of hypoglycaemia.

5 reased weight gain, and high risk for severe hypoglycaemia.

6 r resistance increased in all fetuses during hypoglycaemia.

7 upling and lower the risk of weight gain and hypoglycaemia.

8 o respond to mitochondrial inhibition and to hypoglycaemia.

9 ed insulin secretion even in the presence of hypoglycaemia.

10 ate (measured as ) was almost doubled during hypoglycaemia.

11 ed adrenal responsiveness to insulin-induced hypoglycaemia.

12 c patients is limited by a high frequency of hypoglycaemia.

13 is crucial in the response to hypoxia and to hypoglycaemia.

14 who have difficulty recognising the onset of hypoglycaemia.

15 n people with type 1 diabetes predisposes to hypoglycaemia.

16 We also assessed incidence of severe hypoglycaemia.

17 g or stable rates of hospital admissions for hypoglycaemia.

18 reduce the burden of hospital admissions for hypoglycaemia.

19 ital mortality, and 1 month readmissions for hypoglycaemia.

20 for the global burden of hospitalisation for hypoglycaemia.

21 mpanied by reduced time spent by patients in hypoglycaemia.

22 ey protective mechanism for the organ during hypoglycaemia.

23 ove glycaemic control and reduce the risk of hypoglycaemia.

24 on, inducing weight gain or posing a risk of hypoglycaemia.

25 that is dose-dependent but does not lead to hypoglycaemia.

26 young, type 1 (MODY1) and hyperinsulinaemic hypoglycaemia.

27 .86; p=0.0157), fewer incidences of neonatal hypoglycaemia (0.45; 0.22 to 0.89; p=0.0250), and 1-day

28 on responsiveness to arginine was reduced by hypoglycaemia (0.98 +/- 0.11 ng ml(-1) in H vs. 1.82 +/-

29 .0359), as were rates of nocturnal confirmed hypoglycaemia (1.4 vs 1.8 episodes per patient-year of e

30 recorded during infusion of insulin-induced hypoglycaemia (8-17 mIU kg(-1) min(-1) ) in Alfaxan-anae

31 Fetal pancreatic adaptations to relative hypoglycaemia, a characteristic of intra-uterine growth

32 In adults, hyperinsulinaemic hypoglycaemia accounts for 0.5-5.0% of cases of hypoglyc

33 However, biochemical hypoglycaemia also was increased in the study, which wil

34 During hypoglycaemia, an initial rise in fetal heart rate was f

35 nhibit mTORC1, which coincides with profound hypoglycaemia and a decrease in plasma amino-acid concen

36 estigated individuals with hyperinsulinaemic hypoglycaemia and biochemical or genetic evidence to sug

37 oglycaemia accounts for 0.5-5.0% of cases of hypoglycaemia and can be due either to beta-cell tumours

38 linically, GSDIa is characterized by fasting hypoglycaemia and hepatic glycogen and triglyceride over

39 endocrine tumour who presented with reactive hypoglycaemia and hyperglycaemia, but who was subsequent

40 the p85 alpha isoform are viable but display hypoglycaemia and increased insulin sensitivity correlat

41 o the observations for K(ATP) currents, both hypoglycaemia and inhibition of mitochondrial function e

42 timum diabetes control to reduce the risk of hypoglycaemia and its consequences in advanced type 2 di

43 abetic patients against episodes of profound hypoglycaemia and make the achievement of normoglycaemia

44 ally-occurring fruit-based toxins that cause hypoglycaemia and metabolic derangement.

45 in and placebo groups, with low incidence of hypoglycaemia and no emergence of new safety signals.

46 and biochemical endogenous hyperinsulinaemic hypoglycaemia and no evidence for metastatic disease on

47 eight, and safety outcomes, including severe hypoglycaemia and pulmonary toxicity.

48 t long-term trends in hospital admission for hypoglycaemia and subsequent outcomes in England to help

49 The safety endpoints included hypoglycaemia and uncontrolled hyperglycaemia leading to

50 ed, phrenic neural activity increased during hypoglycaemia and was associated with a significant incr

51 t inhaled insulin has a lower risk of severe hypoglycaemia and weight gain.

52 ds to greater reductions in HbA(1c), weight, hypoglycaemia, and blood pressure than does glimepiride.

53 ell excitability, insulin hypersecretion and hypoglycaemia, and in humans lead to the clinical condit

54 s because it is associated with weight gain, hypoglycaemia, and the need for subcutaneous injections.

55 tes, especially when weight loss and risk of hypoglycaemia are major considerations.

56 m glycaemia without promoting weight gain or hypoglycaemia, are not being undertaken.

57 ted data for all hospital admissions listing hypoglycaemia as primary reason of admission between Jan

58 cacy with low risk of clinically significant hypoglycaemia at any stage in the natural history of typ

59 Hypoglycaemia attenuates cyanide-mediated transcription

60 79 172 people had 101 475 admissions for hypoglycaemia between 2005 and 2014, of which 72 568 (72

61 Insulin (0.4 Ukg(-1)min(-1))-induced hypoglycaemia (blood glucose reduced by ca 50% to 3.4 +/

62 rated, improves glucose control, and reduces hypoglycaemia burden.

63 K(ATP) currents are observed not only during hypoglycaemia, but also in response to mitochondrial inh

64 r the ventilatory hyperpnoea observed during hypoglycaemia by an augmented carotid body and whole bod

65 Hypoglycaemia caused an increase in the counter-regulato

66 oximately 80% of neurones did not respond to hypoglycaemia (changing artificial cerebrospinal fluid (

67 ant-negative CREB inhibitor, exhibit fasting hypoglycaemia [corrected] and reduced expression of gluc

68 Because profound hypoglycaemia does not inhibit mTORC1 in RagA(GTP/GTP) n

69 d orexin neurones in the LH are activated by hypoglycaemia during fasting.

70 (18%) people had more than one admission for hypoglycaemia during the study period.

71 These cells respond to brief hypoglycaemia either with a K(ATP) channel-mediated hype

72 control participants, with comparable severe hypoglycaemia episodes (18 CGM and 21 control) and time

73 in this study is for diagnosing the cases of hypoglycaemia especially in suppression tests of insulin

74 Concomitantly, hypoglycaemia evokes a carotid body-mediated hyperpnoea

75 ion of the cholyl-insulins was the amount of hypoglycaemia following infusion into the small intestin

76 stprandial glucose response to a mixed meal; hypoglycaemia frequency and severity; pulmonary function

77 .5%; -6.9% [-9.8% to -3.9], p<0.0001) and in hypoglycaemia (glucose concentration <3.9 mmol/L; 1.7% v

78 s associated with a decreased risk of severe hypoglycaemia (HR 0.76 [0.65-0.90]; p=0.001).

79 on was associated with: greater awareness of hypoglycaemia in 9 patients, significantly more intense

80 lucose control while alleviating the risk of hypoglycaemia in adults with HbA1c below 7.5% (58 mmol/m

81 dy mass can safely reduce mean glycaemia and hypoglycaemia in adults with type 1 diabetes who were li

82 We assessed rates of hypoglycaemia in all treated patients.

83 -loop systems could reduce risk of nocturnal hypoglycaemia in children and adolescents with type 1 di

84 a role in the counterregulatory response to hypoglycaemia in humans.

85 ay contribute to the development of neonatal hypoglycaemia in macrosomic babies of diabetic mothers.

86 e most common cause of severe and persistent hypoglycaemia in neonates and children.

87 y explains the transient hyperinsulinism and hypoglycaemia in some IUGR infants.

88 of cortisol response was by insulin-induced hypoglycaemia in three cases, by short tetracosactrin te

89 vernight glucose control and reduced risk of hypoglycaemia in type 1 diabetes.

90 ts against neuronal damage caused by hypoxia-hypoglycaemia in vitro and both global and focal cerebra

91 ydrochloride, NCC1048) in a model of hypoxia-hypoglycaemia in vitro and in a gerbil model of global a

92 Hypoglycaemia in vivo induces a counter-regulatory respo

93 Simulated ischemic conditions (hypoxia-hypoglycaemia) in vitro enhanced glutamate efflux from r

94 red for survival, but not for development of hypoglycaemia, in mice lacking p85 alpha.

95 d Charlson comorbidity score) admissions for hypoglycaemia; in admissions for hypoglycaemia per total

96 Advances in the field of hyperinsulinaemic hypoglycaemia include use of rapid molecular genetic tes

97 10 years, hospital admissions in England for hypoglycaemia increased by 39% in absolute terms and by

98 tumour secreting GLP-1 and causing reactive hypoglycaemia, indicates a potential adverse effect of G

99 ageing population, and costs associated with hypoglycaemia, individual and national initiatives shoul

100 measured at baseline, and during acute fetal hypoglycaemia induced by maternal insulin infusion at 12

101 We show that the hypoglycaemia-induced increase in ventilation and CO2 se

102 is revealed that mitochondrial inhibition or hypoglycaemia inhibited an openly rectifying K+ conducta

103 without changes in body-mass index, rate of hypoglycaemia, insulin dose, or circulating concentratio

104 In hyperinsulinaemic hypoglycaemia, insulin secretion becomes dysregulated (i

105 l reports indicate that an increased risk of hypoglycaemia is associated with some GK activators.

106 I cells are direct physiological sensors of hypoglycaemia is challenged by the finding that the basa

107 Hypoglycaemia is counteracted by release of hormones and

108 s and prompt management of hyperinsulinaemic hypoglycaemia is essential to avoid hypoglycaemic brain

109 Hyperinsulinaemic hypoglycaemia is the most common cause of severe and per

110 f GLP-1 to treat diabetes, since the risk of hypoglycaemia is thought to be low.

111 atment rate ratio 0.448, p<0.0001) and minor hypoglycaemia less frequent with liraglutide than with e

112 or a person with diabetes, including fear of hypoglycaemia, loss of glycaemic control, and inadequate

113 evertheless, homozygous mice still displayed hypoglycaemia, lower insulin levels and increased glucos

114 ssive hyperglycaemia (>10 mmol/L) and severe hypoglycaemia (<2.2 mmol/L) should be avoided in critica

115 8.0 mmol/L) (15.9%, 10.7-21.0; p<0.0001) and hypoglycaemia (<3.9 mmol/L) (median 0.9, IQR 0.2-2.2; p=

116 rate glycaemic control), while avoiding mild hypoglycaemia (<3.9 mmol/L), is a reasonable strategy in

117 aximum femoral artery blood flow response to hypoglycaemia occurred earlier in PI50 and PI40 compared

118 Hypoglycaemia occurred in 13 patients (9%) in the sitagl

119 mg, and placebo groups, respectively; severe hypoglycaemia occurred in 21 (8%), 19 (6%), and 19 (7%)

120 Hypoglycaemia occurred in 220 (79%), 235 (79%), and 207

121 Severe hypoglycaemia occurred in one participant in the CGM plu

122 Symptoms of hypoglycaemia occurred in similar proportions of patient

123 ed in either group and one episode of severe hypoglycaemia occurred in the multiple daily injection g

124 No episodes of major hypoglycaemia occurred.

125 ; three trials) and a smaller risk of severe hypoglycaemia (odds ratio 0.61, 95% CI 0.35-0.92; five t

126 om a child with persistent hyperinsulinaemic hypoglycaemia of infancy and been engineered in culture

127 rate interventions given per participant for hypoglycaemia on days 1-5 (ie, glucose <3.9 mmol/L) was

128 iling and sustained hypoxaemia, acidaemia or hypoglycaemia on the fetal cardiovascular responses to a

129 In conclusion, the stimulant effect of hypoglycaemia on the hypoxic ventilatory response is con

130 levels of adrenaline mimicked the effect of hypoglycaemia on ventilation and CO2 sensitivity.

131 ients, grade 3), nausea (one [2%], grade 3), hypoglycaemia (one [2%], grade 3 and one [2%], grade 4),

132 No episodes of severe hypoglycaemia or hyperglycaemia with ketonaemia occurred

133 No episodes of major hypoglycaemia or minor hypoglycaemia were reported.

134 No episodes of serious hypoglycaemia or other serious adverse events occurred.

135 either inhibit ATP production (e.g. hypoxia, hypoglycaemia) or that accelerate ATP consumption (e.g.

136 eprived of either oxygen (hypoxia), glucose (hypoglycaemia), or both oxygen and glucose (ischaemia).

137 ol/L]), but also an increase in CGM-measured hypoglycaemia (p=0.0001 for <70 mg/dL [<3.9 mmol/L], p=0

138 significant differences were seen in severe hypoglycaemia, pancreatitis, pancreatic cancer, or medul

139 Admissions for hypoglycaemia per 100 000 total hospital admissions incr

140 issions for hypoglycaemia; in admissions for hypoglycaemia per total hospital admissions and per diab

141 Rates of overall confirmed hypoglycaemia (plasma glucose <3.1 mmol/L or severe epis

142 Rates of overall confirmed hypoglycaemia (plasma glucose <3.1 mmol/L or severe) wer

143 The hypoglycaemia rate was 0.34 (SE 1.44) and 0.52 (3.01) ev

144 day euglycaemic recovery period from chronic hypoglycaemia reestablished GSIS to normal levels, but t

145 Hypoglycaemia remains an important avoidable iatrogenic

146 men after 32 weeks, with significantly lower hypoglycaemia risk and better patient satisfaction.

147 to be efficacious but in many cases present hypoglycaemia risk due to activation of the enzyme at lo

148 mellitus improved glycaemic control without hypoglycaemia risk.

149 Rates of severe hypoglycaemia seemed similar (0.06 vs 0.05 episodes per

150 We have identified and characterized hypoglycaemia-sensitive neurones in the dorsal vagal com

151 Hypoglycaemia significantly augmented minute ventilation

152 Hypoglycaemia significantly decreased plasma insulin con

153 Across the two trials, rates of confirmed hypoglycaemia (SMBG <3.1 mmol/L or severe [needing assis

154 cells, contribute to the mechanisms by which hypoglycaemia stimulates glucagon release from pancreati

155 ycaemia suppressing the hypoxic response and hypoglycaemia stimulating it.

156 al and symptomatic responses during moderate hypoglycaemia suggest caffeine as a potentially useful t

157 nd cognitive function, and patients recorded hypoglycaemia symptoms on a visual analogue scale.

158 ec, which are associated with lower risks of hypoglycaemia than insulin glargine.

159 o the combined stress of perturbed redox and hypoglycaemia than wild-type cells.

160 der of unregulated insulin secretion despite hypoglycaemia that can occur in isolation or as part of

161 also reduced the proportion of time spent in hypoglycaemia: the proportion of time with glucose conce

162 al contributions of hypoxaemia, acidaemia or hypoglycaemia to mediating these responses can vary.

163 es in ventilation and CO2 sensitivity during hypoglycaemia to prevent a serious acidosis in poorly co

164 n anaesthetized rat model of insulin-induced hypoglycaemia to test the hypothesis that peripheral che

165 For the patient with diabetes, hypoglycaemia unawareness--ie, the warning signs of fall

166 The rate of nocturnal confirmed hypoglycaemia was 25% lower with degludec than with glar

167 ation fetal cardiovascular response to acute hypoglycaemia was consistent with a redistribution of co

168 The rate of nocturnal confirmed hypoglycaemia was higher for IDeg 3TW(AM) than for IGlar

169 Minor hypoglycaemia was recorded in about 5% of participants i

170 Severe or blood glucose-confirmed hypoglycaemia was reported by 16 (4%) participants with

171 Severe hypoglycaemia was reported by two (<1%) participants wit

172 atient per year, respectively, and no severe hypoglycaemia was reported.

173 Hypoglycaemia was the most common adverse event in both

174 The exposure-adjusted rate of overall hypoglycaemia was three times higher in patients given g

175 To mitigate the risk of hypoglycaemia, we sought to increase GK activity by bloc

176 and renal impairment) and the need to avoid hypoglycaemia, weight gain, and drug interactions furthe

177 ncentrations, and occurrence and severity of hypoglycaemia were also similar between groups.

178 ecognition of and physiological responses to hypoglycaemia were altered in patients with insulin-depe

179 No episodes of severe hypoglycaemia were recorded.

180 No episodes of major hypoglycaemia or minor hypoglycaemia were reported.

181 ponse) for counterregulatory hormones during hypoglycaemia were significantly suppressed by hyperoxia

182 t higher degree of glycaemic variability and hypoglycaemia when compared to multiple daily basal-bolu

183 ro-hormonal counterregulation blunted during hypoglycaemia when the carotid bodies were desensitized

184 Tight glycaemic control may result in hypoglycaemia, which in itself can be detrimental.

185 control while lowering the risk of nocturnal hypoglycaemia, which is a major limitation of insulin th

186 rior glycaemic control and increased risk of hypoglycaemia with IDeg 3TW compared with IGlar OD do no

187 dverse effects, and there was no increase in hypoglycaemia with metformin.

188 The improved mean glycaemia and reduced hypoglycaemia with the bionic pancreas relative to insul