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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 dentify associations between metabolites and plasma cortisol, adjusted for potential confounders.
11 in alphaENaC mRNA paralleled the increase in plasma cortisol after delivery, but not T3, and inhibiti
12  effects of proinflammatory stimuli on fetal plasma cortisol also have not been evaluated.
13 0.05), despite comparable increases in fetal plasma cortisol and a similar body weight at birth.
14 othalamic paraventricular nucleus (PVN), and plasma cortisol and ACTH levels, were elevated only duri
15  blood samples were obtained and assayed for plasma cortisol and adrenocorticotropic hormone (ACTH) c
16 xamethasone 1 mg/kg significantly suppressed plasma cortisol and adrenocorticotropic hormone levels c
17 nd renin, and blood pressure correlated with plasma cortisol and AII concentrations.
18  in rodents and sheep report increased fetal plasma cortisol and associated increased gluconeogenesis
19 entially causal associations between morning plasma cortisol and body shape and obesity with inverse-
20  LINC00473 as a genetic link between morning plasma cortisol and body shape.
21 rallelled the normal prepartum rise in fetal plasma cortisol and catecholamines.
22                                              Plasma cortisol and chromogranin A showed a significant
23 nd trunk blood was collected for analysis of plasma cortisol and corticosterone levels.
24 the significant negative correlation between plasma cortisol and CSF CRH levels seen in controls, pat
25                 When all data were combined, plasma cortisol and muscle IGF-I mRNA abundance were inv
26 ternal fasting also induced increases in the plasma cortisol and noradrenaline levels in all the fetu
27                                      Morning plasma cortisol and PER2, BMAL1, and ESR2 expressions in
28 ociative and somaesthetic effects, increased plasma cortisol and prolactin, and reduced resting elect
29                               In conclusion, plasma cortisol and T3 are both required for the late ge
30                                        Fetal plasma cortisol and T3 concentrations were higher in the
31 l treatment groups were combined, both fetal plasma cortisol and T3 concentrations were positively co
32                                              Plasma cortisol and total triiodothyronine (T3) levels i
33 he present study aimed to determine if fetal plasma cortisol and triiodothyronine (T3) influenced the
34 n damage and body condition), physiological (plasma cortisol) and behavioural traits (activity, group
35 on of GR target genes FKBP5, GILZ, and SGK1, plasma cortisol, and childhood trauma.
36                                 Salivary and plasma cortisol, and circadian genes including Clock, Bm
37 ciation with the prepartum increase in fetal plasma cortisol, and treatment of the preterm fetus with
38 re of adrenocorticotropic hormone to augment plasma cortisol appears to be a poor prognostic finding
39                                        Using plasma cortisol as a biomarker for adrenal status (outco
40 lasma catecholamines with their metabolites, plasma cortisol before and after dexamethasone administr
41  (4 microg/kg/min for 6 hrs) that maintained plasma cortisol between 40 and 50 microg/dL, starting 60
42 stream mechanism increases concentrations of plasma cortisol, but the ensuing feedback-inhibited ACTH
43            Naloxone hydrochloride stimulates plasma cortisol by blocking opioidergic input on the cor
44  men (a) antecedent physiologic increases of plasma cortisol can significantly blunt epinephrine, nor
45  daily levels of corticotropin and cortisol; plasma cortisol clearance, metabolism, and production du
46  survival, and lower basal concentrations of plasma cortisol compared with stable animals.
47 s in fetal arterial blood pressure and fetal plasma cortisol concentration as term approaches.
48 se in plasma renin, both correlated with the plasma cortisol concentration before GR138950 treatment.
49 servations from all fetuses were considered, plasma cortisol concentration correlated with plasma AII
50 m, nor the role of the prepartum increase in plasma cortisol concentration in mediating these changes
51 correlation between repeated measurements of plasma cortisol concentration in response to stress.
52 e maintenance of resting blood pressure when plasma cortisol concentration is elevated, whether endog
53  days (2-3 mg kg(-1) day(-1) i.v.) increased plasma cortisol concentration to a value normally seen c
54                                              Plasma cortisol concentration was greater in fetuses at
55      Under basal conditions, twins had lower plasma cortisol concentration, arterial blood pressure a
56 icotropic hormone (ACTH) irrespective of the plasma cortisol concentration, is controversial.
57 correlation between its CSC risk allele with plasma cortisol concentration.
58 n stress response to crowding as measured by plasma cortisol concentration.
59 pendent on preparturient elevations in fetal plasma cortisol concentration.
60 ciation with the prepartum increase in fetal plasma cortisol concentration.
61      Systemic effect was evaluated by hourly plasma cortisol concentrations (8 P.M. to 8 A.M.), 12- a
62 icantly alter blood pressure, heart rate, or plasma cortisol concentrations (all Poverfeeding x sleep
63 ) in fetal sheep at ~0.88 gestation on fetal plasma cortisol concentrations and fetal behaviour [elec
64                                              Plasma cortisol concentrations did not differ between LD
65                                              Plasma cortisol concentrations in an untreated control g
66 4 h urinary free cortisol was 175 nmoles and plasma cortisol concentrations over 24 h showed a normal
67                              Exercise raised plasma cortisol concentrations to 16.9 +/- 1.9 (0930 h)
68             Cortisol infusion elevated fetal plasma cortisol concentrations to values similar to thos
69                          Less suppression of plasma cortisol concentrations was seen in the asthma gr
70  of physiological data using SAS showed that plasma cortisol concentrations were higher (P < 0.01) in
71                              In one patient, plasma cortisol concentrations were measured every 4 h f
72                                              Plasma cortisol concentrations were positively correlate
73 entages in lavage fluid and marginally lower plasma cortisol concentrations.
74 ls), neutrophil function (phagocytosis), and plasma cortisol concentrations.
75 rder exhibited lower baseline and stimulated plasma cortisol concentrations.
76     In untreated and saline-infused fetuses, plasma cortisol correlated with both pulmonary (r = 0.83
77 inhibition on the lysozyme suppression test, plasma cortisol decline on the low-dose (.50 mg) dexamet
78 to determine whether preventing increases in plasma cortisol during antecedent hypoglycemia preserves
79 rated a direct correlation with increases in plasma cortisol during fetal development.
80 e end of the fast and the increment in fetal plasma cortisol during maternal fasting were significant
81 mediates HAAF, we tested the hypothesis that plasma cortisol elevations during euglycemia that are co
82 ied to date, the prepartum increase in fetal plasma cortisol has an important role in the maturation
83       The effects of nicotine on subjective, plasma cortisol, heart rate, and systolic and diastolic
84 NE, plasma NE, plasma epinephrine (EPI), and plasma cortisol hourly for 30 h.
85 ibited significant IL-2-induced increases in plasma cortisol, IL-6, and depressive symptoms (p<0.05),
86                                   Peripheral plasma cortisol increased from 250 +/- 119 nmol/L at 0 m
87  sheep occurred without an increase in fetal plasma cortisol, indicating that endotoxin promoted lung
88 es was not clearly related to any changes in plasma cortisol, insulin, triiodothyronine, IGF-1 or glu
89  to determine whether antecedent increase of plasma cortisol is a mechanism responsible for this find
90 oss species, the prepartum increase in fetal plasma cortisol is responsible for maturing a number of
91 ia and (b) these data suggest that increased plasma cortisol is the mechanism responsible for anteced
92 of cortisol values after dexamethasone 1 mg (plasma cortisol less than 83 nmol/L).
93 enge significantly increased rectal temp and plasma cortisol level in all treatment groups.
94 ary outcome GIAI was defined as a stimulated plasma cortisol level less than 420 nmol/L in response t
95 d objective (blood pressure, pulse rate, and plasma cortisol level) measures of intoxication were tak
96 depressive reaction correlated with baseline plasma cortisol levels (r = 0.59; P =.04).
97     11B-HSD1 availability was not related to plasma cortisol levels (R2 = 0.026, P = 0.37).
98                                              Plasma cortisol levels 3 and 7 days later, and measures
99        No associations were observed between plasma cortisol levels and clinical and cognitive assess
100 cemia; (b) hypoglycemia-induced increases in plasma cortisol levels are a major mechanism responsible
101         In addition, endogenous increases in plasma cortisol levels are associated with decreases in
102                                        Fetal plasma cortisol levels at the end of the fast and the in
103 cortisol cut-off values were 0.015mug/dL for plasma cortisol levels below 3mug/dL (sensitivity 83%, s
104 and after experimental manipulation of fetal plasma cortisol levels by fetal adrenalectomy and exogen
105 and after experimental manipulation of fetal plasma cortisol levels by fetal adrenalectomy and exogen
106 support the study hypothesis that changes in plasma cortisol levels can be classically conditioned in
107   To test the hypothesis that alterations in plasma cortisol levels can be conditioned in humans, the
108 axine-exposed group had significantly higher plasma cortisol levels compared to the subordinate fish
109                                However, once plasma cortisol levels exceeded 17.5 ng ml-1, plasma cat
110                                         Mean plasma cortisol levels following treatment were reduced
111 ved in several infectious diseases, and high plasma cortisol levels have also been found in human vis
112 in antisocial males, we investigated morning plasma cortisol levels in adolescent girls with conduct
113 elation between salivary cortisol levels and plasma cortisol levels in all patients, patients under a
114                     We evaluated the role of plasma cortisol levels in determining sodium lactate-ind
115 tisol levels were positively correlated with plasma cortisol levels in pediatric asthmatic patients.
116 study was to determine the role of increased plasma cortisol levels in the pathogenesis of hypoglycem
117 ounted for an increase by a factor of 3.5 in plasma cortisol levels in the patients, as compared with
118 c-pituitary-adrenal (HPA) axis with elevated plasma cortisol levels is characteristic of acute major
119 ndrome is defined as a prolonged increase in plasma cortisol levels that is not due to a physiologica
120 patients had significantly higher CSF NE and plasma cortisol levels that were increased around the cl
121 a, but not in those without dementia, higher plasma cortisol levels were associated with more rapidly
122                        In G. monasteriensis, plasma cortisol levels were lower when with the mother t
123           When all data were combined, fetal plasma cortisol levels were positively correlated to ute
124                                      Morning plasma cortisol levels were significantly diminished in
125             Diurnal variations in CSF NE and plasma cortisol levels were virtually superimposable and
126 ituitary-adrenal (HPA) axis activation (high plasma cortisol levels) and evidence of hyperventilation
127 Cushing's disease, characterized by elevated plasma cortisol levels, can be controlled by inhibition
128 gher HPA activity, as reflected by increased plasma cortisol levels, is associated with more rapid di
129 ly, close correlations were discovered among plasma cortisol levels, TSC22D3 expression in circulatin
130   Hydrocortisone led to an acute increase in plasma cortisol levels.
131 o 15 d had no significant elevations in cord plasma cortisol levels.
132 p, lipopolysaccharide increased cytokine and plasma cortisol levels.
133 taining in the samples correlated with basal plasma cortisol levels.
134 n levels were unrelated to dominance rank or plasma cortisol levels.
135  and reproductive characteristics as well as plasma cortisol levels.
136              For 432 subjects PRS scores for plasma cortisol, major depression, and neuroticism were
137 which indicate the significance of the first plasma cortisol measurement in defining the trait.
138                                              Plasma cortisol measurements at baseline and 3 months we
139 in barrier function, as well as increases in plasma cortisol, norepinephrine, interleukin-1beta and i
140 with cortisol infused to stimulate levels of plasma cortisol occurring during clamped hypoglycemia (5
141 tropin (250 mug) administration and a random plasma cortisol of < 10 mug/dL may be used by clinicians
142 ma NE (P < 0.02), plasma EPI (P < 0.02), and plasma cortisol (P < 0.02).
143  infusion increased maternal, but not fetal, plasma cortisol (P < 0.05).
144 st, there were large circadian variations in plasma cortisol (peak-to-trough approximately 85% of mea
145 re observed in physiological rhythms such as plasma cortisol, plasma melatonin and core temperature d
146 n HPA axis activation, resulting in elevated plasma cortisol production and plasma concentrations.
147        Statin therapy does not influence the plasma cortisol profiles in patients with severe sepsis.
148 e, heart rate, body temperature, pupil size, plasma cortisol, prolactin, oxytocin, and epinephrine.
149                                      Morning plasma cortisol proxied by rs7450600 was associated posi
150                       Only in women, morning plasma cortisol (proxied by ten genetic polymorphisms) w
151     Correlation analysis revealed that fetal plasma cortisol rather than gestational age was a greate
152 ery selective social buffering effect on the plasma cortisol response in a nonmonogamous species.
153 ffect of different classes of females on the plasma cortisol response of male guinea pigs (Cavia porc
154                                          The plasma cortisol response to endotoxemia on day 2 was sim
155                         Group differences in plasma cortisol response to separation from the mother a
156 ar females did not differentially reduce the plasma cortisol response.
157                                              Plasma cortisol responses to IL-6 did not differ signifi
158  administration of 1 microg/kg ovine CRF and plasma cortisol responses to the administration of 250 m
159 al prefrontal cortex that also covaried with plasma cortisol, suggesting an influence on stress respo
160 tal group had significantly higher levels of plasma cortisol than the control group, after controllin
161 saturable phenomenon at the concentration of plasma cortisol that is normally achieved after surgery
162                       Whether they impact on plasma cortisol through inhibition of cholesterol synthe
163                                 Responses of plasma cortisol to dexamethasone, CRH stimulation, and m
164 the hypothesis that a transient elevation of plasma cortisol to stress-associated levels would enhanc
165 kg-1 day-1) at either 113 or 129 days raised plasma cortisol to the level seen near term and caused a
166 gns of Cushing's syndrome were observed, and plasma cortisol values did not differ significantly from
167                                 This rise in plasma cortisol was accompanied by increases in blood pr
168                                              Plasma cortisol was assessed repetitively before and aft
169                                              Plasma cortisol was elevated in fetuses of MNR mothers (
170 ortisol and total catecholamines showed that plasma cortisol was the predominant regulator of fetal g
171        In marked contrast, when increases of plasma cortisol were prevented in the patient group, day
172 pport a causal association of higher morning plasma cortisol with larger waist size in women and high

 
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