ライフサイエンスコーパス: plasma cortisol

1 ent increase in temperature, heart rate, and plasma cortisol.

2 llel with the normal prepartum rise in fetal plasma cortisol.

3 NR3C1 (P=0.04); and 33% lower (P=0.07) cord plasma cortisol.

4 ted in further twofold greater elevations of plasma cortisol.

5 evels and a single time point measurement of plasma cortisol.

6 n parallel with the normal prepartum rise in plasma cortisol.

7 l age in parallel with the prepartum rise in plasma cortisol.

8 Hypoglycemia increased plasma cortisol (3-fold to 14.3+/-1 mg/dl) and epinephri

9 ors sought to determine whether increases in plasma cortisol, a marker of HPA activity, were associat

10 in alphaENaC mRNA paralleled the increase in plasma cortisol after delivery, but not T3, and inhibiti

11 effects of proinflammatory stimuli on fetal plasma cortisol also have not been evaluated.

12 othalamic paraventricular nucleus (PVN), and plasma cortisol and ACTH levels, were elevated only duri

13 xamethasone 1 mg/kg significantly suppressed plasma cortisol and adrenocorticotropic hormone levels c

14 nd renin, and blood pressure correlated with plasma cortisol and AII concentrations.

15 in rodents and sheep report increased fetal plasma cortisol and associated increased gluconeogenesis

16 rallelled the normal prepartum rise in fetal plasma cortisol and catecholamines.

17 Plasma cortisol and chromogranin A showed a significant

18 nd trunk blood was collected for analysis of plasma cortisol and corticosterone levels.

19 the significant negative correlation between plasma cortisol and CSF CRH levels seen in controls, pat

20 When all data were combined, plasma cortisol and muscle IGF-I mRNA abundance were inv

21 ternal fasting also induced increases in the plasma cortisol and noradrenaline levels in all the fetu

22 ociative and somaesthetic effects, increased plasma cortisol and prolactin, and reduced resting elect

23 In conclusion, plasma cortisol and T3 are both required for the late ge

24 Fetal plasma cortisol and T3 concentrations were higher in the

25 l treatment groups were combined, both fetal plasma cortisol and T3 concentrations were positively co

26 Plasma cortisol and total triiodothyronine (T3) levels i

27 he present study aimed to determine if fetal plasma cortisol and triiodothyronine (T3) influenced the

28 on of GR target genes FKBP5, GILZ, and SGK1, plasma cortisol, and childhood trauma.

29 ciation with the prepartum increase in fetal plasma cortisol, and treatment of the preterm fetus with

30 re of adrenocorticotropic hormone to augment plasma cortisol appears to be a poor prognostic finding

31 lasma catecholamines with their metabolites, plasma cortisol before and after dexamethasone administr

32 (4 microg/kg/min for 6 hrs) that maintained plasma cortisol between 40 and 50 microg/dL, starting 60

33 stream mechanism increases concentrations of plasma cortisol, but the ensuing feedback-inhibited ACTH

34 Naloxone hydrochloride stimulates plasma cortisol by blocking opioidergic input on the cor

35 men (a) antecedent physiologic increases of plasma cortisol can significantly blunt epinephrine, nor

36 daily levels of corticotropin and cortisol; plasma cortisol clearance, metabolism, and production du

37 survival, and lower basal concentrations of plasma cortisol compared with stable animals.

38 s in fetal arterial blood pressure and fetal plasma cortisol concentration as term approaches.

39 se in plasma renin, both correlated with the plasma cortisol concentration before GR138950 treatment.

40 servations from all fetuses were considered, plasma cortisol concentration correlated with plasma AII

41 m, nor the role of the prepartum increase in plasma cortisol concentration in mediating these changes

42 correlation between repeated measurements of plasma cortisol concentration in response to stress.

43 e maintenance of resting blood pressure when plasma cortisol concentration is elevated, whether endog

44 days (2-3 mg kg(-1) day(-1) i.v.) increased plasma cortisol concentration to a value normally seen c

45 Plasma cortisol concentration was greater in fetuses at

46 Under basal conditions, twins had lower plasma cortisol concentration, arterial blood pressure a

47 icotropic hormone (ACTH) irrespective of the plasma cortisol concentration, is controversial.

48 n stress response to crowding as measured by plasma cortisol concentration.

49 pendent on preparturient elevations in fetal plasma cortisol concentration.

50 ciation with the prepartum increase in fetal plasma cortisol concentration.

51 Systemic effect was evaluated by hourly plasma cortisol concentrations (8 P.M. to 8 A.M.), 12- a

52 Plasma cortisol concentrations did not differ between LD

53 Plasma cortisol concentrations in an untreated control g

54 4 h urinary free cortisol was 175 nmoles and plasma cortisol concentrations over 24 h showed a normal

55 Exercise raised plasma cortisol concentrations to 16.9 +/- 1.9 (0930 h)

56 Cortisol infusion elevated fetal plasma cortisol concentrations to values similar to thos

57 Less suppression of plasma cortisol concentrations was seen in the asthma gr

58 In one patient, plasma cortisol concentrations were measured every 4 h f

59 Plasma cortisol concentrations were positively correlate

60 entages in lavage fluid and marginally lower plasma cortisol concentrations.

61 ls), neutrophil function (phagocytosis), and plasma cortisol concentrations.

62 rder exhibited lower baseline and stimulated plasma cortisol concentrations.

63 In untreated and saline-infused fetuses, plasma cortisol correlated with both pulmonary (r = 0.83

64 inhibition on the lysozyme suppression test, plasma cortisol decline on the low-dose (.50 mg) dexamet

65 to determine whether preventing increases in plasma cortisol during antecedent hypoglycemia preserves

66 rated a direct correlation with increases in plasma cortisol during fetal development.

67 e end of the fast and the increment in fetal plasma cortisol during maternal fasting were significant

68 mediates HAAF, we tested the hypothesis that plasma cortisol elevations during euglycemia that are co

69 ied to date, the prepartum increase in fetal plasma cortisol has an important role in the maturation

70 The effects of nicotine on subjective, plasma cortisol, heart rate, and systolic and diastolic

71 NE, plasma NE, plasma epinephrine (EPI), and plasma cortisol hourly for 30 h.

72 ibited significant IL-2-induced increases in plasma cortisol, IL-6, and depressive symptoms (p<0.05),

73 Peripheral plasma cortisol increased from 250 +/- 119 nmol/L at 0 m

74 sheep occurred without an increase in fetal plasma cortisol, indicating that endotoxin promoted lung

75 es was not clearly related to any changes in plasma cortisol, insulin, triiodothyronine, IGF-1 or glu

76 to determine whether antecedent increase of plasma cortisol is a mechanism responsible for this find

77 oss species, the prepartum increase in fetal plasma cortisol is responsible for maturing a number of

78 ia and (b) these data suggest that increased plasma cortisol is the mechanism responsible for anteced

79 of cortisol values after dexamethasone 1 mg (plasma cortisol less than 83 nmol/L).

80 d objective (blood pressure, pulse rate, and plasma cortisol level) measures of intoxication were tak

81 depressive reaction correlated with baseline plasma cortisol levels (r = 0.59; P =.04).

82 Plasma cortisol levels 3 and 7 days later, and measures

83 No associations were observed between plasma cortisol levels and clinical and cognitive assess

84 cemia; (b) hypoglycemia-induced increases in plasma cortisol levels are a major mechanism responsible

85 In addition, endogenous increases in plasma cortisol levels are associated with decreases in

86 Fetal plasma cortisol levels at the end of the fast and the in

87 and after experimental manipulation of fetal plasma cortisol levels by fetal adrenalectomy and exogen

88 and after experimental manipulation of fetal plasma cortisol levels by fetal adrenalectomy and exogen

89 support the study hypothesis that changes in plasma cortisol levels can be classically conditioned in

90 To test the hypothesis that alterations in plasma cortisol levels can be conditioned in humans, the

91 axine-exposed group had significantly higher plasma cortisol levels compared to the subordinate fish

92 However, once plasma cortisol levels exceeded 17.5 ng ml-1, plasma cat

93 Mean plasma cortisol levels following treatment were reduced

94 in antisocial males, we investigated morning plasma cortisol levels in adolescent girls with conduct

95 We evaluated the role of plasma cortisol levels in determining sodium lactate-ind

96 study was to determine the role of increased plasma cortisol levels in the pathogenesis of hypoglycem

97 ounted for an increase by a factor of 3.5 in plasma cortisol levels in the patients, as compared with

98 c-pituitary-adrenal (HPA) axis with elevated plasma cortisol levels is characteristic of acute major

99 patients had significantly higher CSF NE and plasma cortisol levels that were increased around the cl

100 a, but not in those without dementia, higher plasma cortisol levels were associated with more rapidly

101 In G. monasteriensis, plasma cortisol levels were lower when with the mother t

102 When all data were combined, fetal plasma cortisol levels were positively correlated to ute

103 Morning plasma cortisol levels were significantly diminished in

104 Diurnal variations in CSF NE and plasma cortisol levels were virtually superimposable and

105 ituitary-adrenal (HPA) axis activation (high plasma cortisol levels) and evidence of hyperventilation

106 Cushing's disease, characterized by elevated plasma cortisol levels, can be controlled by inhibition

107 gher HPA activity, as reflected by increased plasma cortisol levels, is associated with more rapid di

108 o 15 d had no significant elevations in cord plasma cortisol levels.

109 p, lipopolysaccharide increased cytokine and plasma cortisol levels.

110 taining in the samples correlated with basal plasma cortisol levels.

111 n levels were unrelated to dominance rank or plasma cortisol levels.

112 and reproductive characteristics as well as plasma cortisol levels.

113 For 432 subjects PRS scores for plasma cortisol, major depression, and neuroticism were

114 which indicate the significance of the first plasma cortisol measurement in defining the trait.

115 Plasma cortisol measurements at baseline and 3 months we

116 in barrier function, as well as increases in plasma cortisol, norepinephrine, interleukin-1beta and i

117 with cortisol infused to stimulate levels of plasma cortisol occurring during clamped hypoglycemia (5

118 tropin (250 mug) administration and a random plasma cortisol of < 10 mug/dL may be used by clinicians

119 ma NE (P < 0.02), plasma EPI (P < 0.02), and plasma cortisol (P < 0.02).

120 infusion increased maternal, but not fetal, plasma cortisol (P < 0.05).

121 st, there were large circadian variations in plasma cortisol (peak-to-trough approximately 85% of mea

122 re observed in physiological rhythms such as plasma cortisol, plasma melatonin and core temperature d

123 n HPA axis activation, resulting in elevated plasma cortisol production and plasma concentrations.

124 Statin therapy does not influence the plasma cortisol profiles in patients with severe sepsis.

125 e, heart rate, body temperature, pupil size, plasma cortisol, prolactin, oxytocin, and epinephrine.

126 Correlation analysis revealed that fetal plasma cortisol rather than gestational age was a greate

127 ery selective social buffering effect on the plasma cortisol response in a nonmonogamous species.

128 ffect of different classes of females on the plasma cortisol response of male guinea pigs (Cavia porc

129 The plasma cortisol response to endotoxemia on day 2 was sim

130 Group differences in plasma cortisol response to separation from the mother a

131 ar females did not differentially reduce the plasma cortisol response.

132 Plasma cortisol responses to IL-6 did not differ signifi

133 administration of 1 microg/kg ovine CRF and plasma cortisol responses to the administration of 250 m

134 tal group had significantly higher levels of plasma cortisol than the control group, after controllin

135 saturable phenomenon at the concentration of plasma cortisol that is normally achieved after surgery

136 Whether they impact on plasma cortisol through inhibition of cholesterol synthe

137 Responses of plasma cortisol to dexamethasone, CRH stimulation, and m

138 the hypothesis that a transient elevation of plasma cortisol to stress-associated levels would enhanc

139 kg-1 day-1) at either 113 or 129 days raised plasma cortisol to the level seen near term and caused a

140 gns of Cushing's syndrome were observed, and plasma cortisol values did not differ significantly from

141 This rise in plasma cortisol was accompanied by increases in blood pr

142 Plasma cortisol was assessed repetitively before and aft

143 Plasma cortisol was elevated in fetuses of MNR mothers (

144 ortisol and total catecholamines showed that plasma cortisol was the predominant regulator of fetal g

145 In marked contrast, when increases of plasma cortisol were prevented in the patient group, day