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Background: Cam deformities cause femoroacetabular impingement and damage the acetabular labral-chondral complex. The aims of this study were to investigate the potential of delayed gadolinium-enhanced magnetic resonance imaging of cartilage (dGEMRIC) to detect cartilage disease in asymptomatic hips with cam deformities compared with morphologically normal hips, establish whether dGEMRIC could identify advanced disease in hips with positive clinical findings, and establish whether cartilage damage correlated with the severity of the cam deformity.Methods: Subjects were recruited from a prospective study of individuals with a family history of osteoarthritis and their spouses who served as control subjects. Their symptoms and impingement test results were recorded. Asymptomatic hips with normal radiographic joint-space width were placed in a subgroup according to the presence of a cam deformity and the impingement test result. dGEMRIC was performed on a 3-T system, studying two regions of interest: the anterosuperior aspect of the acetabular cartilage (T1(acet)) and the total femoral and acetabular cartilage (T1(total)). The ratio T1(acet)/T1(total) gave the relative glycosaminoglycan content in the anterosuperior aspect of the acetabular cartilage. The cohort was placed in subgroups by joint morphology, impingement test status, and genetic predisposition; the mean T1 scores were compared, and the alpha angle and T1 were correlated.Results: Of thirty-two subjects (mean age, fifty-two years), nineteen had cam deformities. Hips with a cam deformity had reduced acetabular glycosaminoglycan content compared with normal hips (mean T1(acet)/T1(total), 0.949 and 1.093, respectively; p = 0.0008). Hips with a positive impingement test result had global depletion of glycosaminoglycan compared with hips with a negative result (mean T1(total), 625 ms versus 710 ms; p = 0.0152). T1(acet) inversely correlated with the magnitude of the alpha angle (r = -0.483, p = 0.0038), suggesting that the severity of cartilage damage correlates with the magnitude of the cam deformity. All of these differences occurred irrespective of genetic predisposition.Conclusions: The dGEMRIC technique can detect cartilage damage in asymptomatic hips with cam deformities and no radiographic evidence of joint space narrowing. This damage correlates with cam deformity severity. Further study of the application of dGEMRIC as an imaging biomarker of early osteoarthritis is justified to validate its prognostic accuracy, identify subjects for clinical trials, and evaluate the effectiveness of surgical procedures. [ABSTRACT FROM AUTHOR]

BACKGROUND: Threonine is an indispensable amino acid with a complex degradative pathway. Use of the indicator amino acid oxidation technique should provide an estimate of the threonine requirement that is not affected by its metabolic pathway. OBJECTIVE: Our objective was to determine the requirement for threonine in men by using the indicator amino acid oxidation method and to provide statistical estimates of the population mean and 95% CIs of the threonine requirement. We hypothesized that the current World Health Organization estimate of the threonine requirement, 7 mg x kg(-)(1) x d(-)(1) (based on nitrogen balance studies), is too low. DESIGN: Six healthy men each received 6 different threonine intakes while consuming an energy-sufficient diet with 1.0 g L-amino acid mixture x kg(-)(1) x d(-)(1). The effect of graded alterations in dietary threonine intake on phenylalanine flux and oxidation was studied by using L-[1-(13)C]phenylalanine as the indicator amino acid. RESULTS: The results of two-phase linear regression crossover analysis showed that the mean threonine requirement, based on indicator oxidation, was 19.0 mg x kg(-)(1) x d(-)(1) with an upper safe intake of 26.2 mg x kg(-)(1) x d(-)(1). CONCLUSIONS: This is the first application of the indicator amino acid oxidation technique in humans to study the requirement for an indispensable amino acid with a complex degradative pathway. We found that the upper safe intake for 95% of the population is almost 4-fold higher than the current World Health Organization estimate. Copyright © 2000 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]

Aims: To improve energy intake in sick very low birthweight (VLBW) infants; to decrease growth problems, lessen pulmonary morbidity, shorten hospital stay, and avoid possible feeding related morbidity. Morbidity in VLBW infants thought to be associated with parenteral and enteral feeding includes bronchopulmonary dysplasia, necrotising enterocolitis, septicaemia, cholestasis and osteopenia of prematurity.Methods: A prospective randomised controlled trial (RCT) comparing two types of nutritional intervention was performed involving 125 sick VLBW infants in the setting of a regional neonatal intensive care unit. Babies were randomly allocated to either an aggressive nutritional regimen (group A) or a control group (group B). Babies in group B received a conservative nutritional regimen while group A received a package of more aggressive parenteral and enteral nutrition. Statistical analysis was done using Student's t test, the Mann-Whitney U test, the chi 2 test and logistic regression.Results: There was an excess of sicker babies in group A, as measured by initial disease severity (P < 0.01), but mean total energy intakes were significantly higher (P < 0.001) in group A at days 3 to 42 while receiving total or partial parenteral nutrition. Survival and the incidences of bronchopulmonary dysplasia, septicaemia, cholestasis, osteopenia and necrotising enterocolitis were similar in both groups. Growth in early life and at discharge from hospital was significantly better in babies in group A. There were no decreases in pulmonary morbidity or hospital stay.Conclusion: Nutritional intake in sick VLBW infants can be improved without increasing the risk of adverse clinical or metabolic sequelae. Improved nutritional intake resulted in better growth, both in discharge, but did not decrease pulmonary morbidity or shorten hospital stay. [ABSTRACT FROM AUTHOR]