The Barker model of the in utero origins of diminished muscle mass in those born small invokes the adaptive "sparing" of brain tissue development at the expense of muscle. Though compelling, to date this model has not been directly tested. This article develops an allometric framework for testing the principal prediction of the Barker model-that among those born small muscle mass is sacrificed to spare brain growth-then evaluates this hypothesis using data from the third National Health and Nutrition Examination Survey (NHANES III). The results indicate clear support for a negative relationship between the allometric development of the two tissues; however, a further consideration of conserved mammalian fetal circulatory patterns suggests the possibility that system-constrained patterns of developmental damage and "bet-hedging" responses in affected tissues may provide a more adequate explanation of the results. Far from signaling the end of studies of adaptive developmental programming, this perspective may open a promising new avenue of inquiry within the fields of human biology and the developmental origins of health and disease.
In a study to determine the prevalence of urinary tract infections (UTI) in primary biliary cirrhosis, midstream specimens of urine from 97 females with primary biliary cirrhosis and 85 females with other chronic liver diseases were investigated prospectively for urinary pathogens and Mycobacterium gordonae. No significant differences between primary biliary cirrhosis and the two groups were observed in the prevalence of significant bacteriuria (11.3% vs. 7.1%), the prevalence of Escherichia coli UTI (9.3% vs. 7.1%) or the colony morphology of Escherichia coli. No mycobacterial species were grown from any sample. In both groups, the prevalence of UTI was higher in patients with cirrhosis (20% in both) than in those without.
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