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Cincinnati, OH, United States

Grubenhoff J.A.,University of Colorado at Denver | Kirkwood M.,University of Colorado at Denver | Gao D.,Clinical Translational Research Center | Deakyne S.,University of Colorado at Denver | Wathen J.,University of Colorado at Denver
Pediatrics | Year: 2010

OBJECTIVE: The Standardized Assessment of Concussion (SAC) is a validated tool for identifying the effects of mild traumatic brain injury (mTBI). Previous research focused on sport-related sideline evaluation of adolescents and adults. Our goal was to evaluate performance of the SAC among subjects with and without head injury in a pediatric emergency department (ED). METHODS: This was an observational study of children 6 to 18 years of age who presented to an ED with blunt head injury (case-patients) or minor extremity injury (controls). SAC and graded-symptom-checklist scores were compared. American Academy of Neurology concussion grades, presence of loss of consciousness and posttraumatic amnesia were also compared with SAC and graded-symptom-checklist scores among case-patients. RESULTS: Three hundred forty-eight children were enrolled. SAC scores trended lower (greater cognitive deficits) for case-patients compared with controls but did not reach significance. Graded-symptom-checklist scores were significantly higher among case-patients. Presence of altered mental status magnified this effect. There was no correlation between SAC scores and other indicators of mTBI. There was a positive correlation between graded-symptom-checklist scores and posttraumatic amnesia and American Academy of Neurology concussion grade. CONCLUSIONS: The graded symptom checklist reliably identified mTBI symptoms for all children aged 6 years and older. SAC scores tended to be lower for case-patients compared with controls but did not reach signifi-cance. Patients with altered mental status at the time of injury manifest an increased number and severity of symptoms. Additional research into strategies to identify cognitive deficits related to mTBI and classify mTBI severity in children is needed. Copyright © 2010 by the American Academy of Pediatrics. Source


Tong J.,University of Cincinnati | Davis H.W.,University of Cincinnati | Summer S.,Clinical Translational Research Center | Benoit S.C.,University of Cincinnati | And 6 more authors.
Diabetes | Year: 2014

Unacylated ghrelin (UAG) is the predominant ghrelin isoform in the circulation. Despite its inability to activate the classical ghrelin receptor, preclinical studies suggest that UAG may promote β-cell function. We hypothesized that UAG would oppose the effects of acylated ghrelin (AG) on insulin secretion and glucose tolerance. AG (1 μg/ kg/h), UAG (4 μg/kg/h), combined AG+UAG, or saline were infused to 17 healthy subjects (9 men and 8 women) on four occasions in randomized order. Ghrelin was infused for 30 min to achieve steady-state levels and continued through a 3-h intravenous glucose tolerance test. The acute insulin response to glucose (AIRg), insulin sensitivity index (SI), disposition index (DI), and intravenous glucose tolerance (kg) were compared for each subject during the four infusions. AG infusion raised fasting glucose levels but had no effect on fasting plasma insulin. Compared with the saline control, AG and AG+UAG both decreased AIRg, but UAG alone had no effect. SI did not differ among the treatments. AG, but not UAG, reduced DI and kg and increased plasma growth hormone. UAG did not alter growth hormone, cortisol, glucagon, or free fatty acid levels. UAG selectively decreased glucose and fructose consumption compared with the other treatments. In contrast to previous reports, acute administration of UAG does not have independent effects on glucose tolerance or β-cell function and neither augments nor antagonizes the effects of AG. © 2014 by the American Diabetes Association. Source


Meier J.J.,Ruhr University Bochum | Pennartz C.,Ruhr University Bochum | Schenker N.,Ruhr University Bochum | Menge B.A.,Ruhr University Bochum | And 4 more authors.
Diabetes, Obesity and Metabolism | Year: 2013

Aim: Postprandial insulin pulsatility is impaired in patients with type 2 diabetes, but the effects of exogenous insulin therapy on pulsatile insulin secretion are not known. We addressed, whether pulsatile insulin secretion is related to glycaemic control, whether basal insulin supplementation increases postprandial insulin secretion, and if so, is this accomplished by a specific improvement in pulsatile insulin secretion? Methods: Fourteen patients with type 2 diabetes underwent a mixed meal test before and after an 8-week treatment period with insulin glargine. Glucose, insulin and C-peptide levels were measured, and insulin pulsatility was determined by deconvolution analysis. Results: Insulin treatment lowered fasting glycaemia from 179.6±7.5mg/dl to 117.6±6.5mg/dl (p<0.001). Postprandial insulin and C-peptide levels increased significantly after the treatment period (p<0.0001). The total calculated insulin secretion rate increased with insulin treatment (p=0.0039), with non-significant increases in both pulsatile and non-pulsatile insulin secretion. Insulin pulse frequency was unchanged by the intervention. There was an inverse relationship between fasting and postprandial glycaemia and insulin pulse mass (r2=0.51 and 0.56, respectively), whereas non-pulsatile insulin secretion was unrelated to either fasting or postprandial glucose concentrations (r2=0.0073 and 0.031). Conclusions: Hyperglycaemia in type 2 diabetes is associated with a reduction in postprandial insulin secretion, specifically through a reduction in insulin pulsatility. Reducing chronic hyperglycaemia by basal insulin therapy enhances endogenous β-cell function in the postprandial state. These data support the use of basal insulin regimens in the pharmacotherapy of overtly hyperglycaemic patients with type 2 diabetes. © 2012 Blackwell Publishing Ltd. Source


Summer S.S.,Clinical Translational Research Center | Pratt J.M.,Cincinnati Childrens Hospital Medical Center | Koch E.A.,Cincinnati Childrens Hospital Medical Center | Anderson J.B.,Heart Institute
Respiratory Care | Year: 2014

BACKGROUND: Sleeping metabolic rate (SMR) is used as a proxy for basal metabolic rate in infants, when measurement while awake is not practical. Measuring SMR via indirect calorimetry (IC) can be useful for assessing feeding adequacy especially in compromised neonates. Standard IC equipment, including a hood placed over the head, is not designed for the smallest of patients. Our aim was to determine whether a nonstandard smaller hood measures SMR in neonates similarly compared with a standard large hood. METHODS: SMR was measured in healthy neonates (controls) and those born with single-ventricle congenital heart disease (cases). Two measurements were performed: SMR using a standard larFĒCO2ge hood and SMR using a smaller hood. Time-to-steady state, minute ventilation (V̇E), and fraction of exhaled carbon dioxide (FECO2; an indicator of data quality) were also measured. Primary outcome was SMR using both hoods. Results are stated as median (interquartile range). Spearman's correlations measured association between the small and large hoods. RESULTS: We studied 9 controls and 7 cases. SMR in controls was not different between the small and large hoods (35.7 [15.14] vs 37.8 [7.41] kcal/kg/d, respectively). In cases, SMR with the small hood was significantly greater than that with the large hood (45.5 [4.63] vs 34.2 [8] kcal/kg/d, P < .02). FECO2 was significantly higher with the small hood versus the large hood in both groups, and V̇E was significantly lower with the small hood versus the large hood in controls only. The SMRs with the small and large hoods were significantly correlated in the control group (r = 0.80, P < .01). Time-to-steady state was similar in both groups regardless of hood size. CONCLUSIONS: SMR measured with a small hood yields results similar to those measured with a large hood in healthy neonates without affecting testing time or other aspects of the IC procedure. Furthermore, results in compromised infants suggest that a smaller hood may facilitate SMR testing in this population. © 2014 by Daedalus Enterprises. Source


Roelfsema F.,Leiden University | Pijl H.,Leiden University | Keenan D.M.,University of Virginia | Veldhuis J.D.,Clinical Translational Research Center
European Journal of Endocrinology | Year: 2012

Background: The ACTH-cortisol axis in women is activated and associated with decreased ACTH potency, estimated by relating ACTH and cortisol pulse masses. Recently, a new accurate method for constructing the endogenous dose-response relationship was introduced, which is based on the relation between ACTH concentrations and associated cortisol secretion rates within cortisol bursts. Hypothesis: The endogenous dose-response relation between ACTH and cortisol in obesity is changed, leading to diminished responsiveness. Subjects: Twenty-five obese premenopausal women and 16 normal weight premenopausal women were studied by 10-min blood sampling for 24 h. Outcomes: ACTH and cortisol secretion rates, analytical dose-response estimates of endogenous ACTH efficacy (maximal cortisol secretion), dynamic ACTH potency, and adrenal sensitivity (slope term) from 24-h ACTH-cortisol profiles were quantified. Results: The initial potency (negative logarithm) was -7.83±0.75 (mean±S.E.M.) in obese women and -10.14±1.08 in lean women (P=0.10), and the corresponding values for the recovery phase were -26.62±2.21 and -36.67±1.66 (P=0.004). The sensitivity (curve slope) amounted to 0.468±0.05 in obese women and 0.784±0.09 in normal weight women (P=0.004). The efficacy (maximal value) was 17.6±4.9 nmol/l per min in obese women and 26.3±3.8 nmol/l per min in normal weight women (P=0.009). Basal secretion rate, inflection point, and EC 50 values were not different. Bromocriptine or acipimox did not change the dose-response curve. Conclusion: The ACTH-cortisol relation in obesity in women is characterized by decreased sensitivity and efficacy, thus explaining non-elevated serum cortisol concentrations despite increased plasma ACTH levels. © 2012 European Society of Endocrinology. Source

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