Neurturin enhances the recovery of erectile function following bilateral cavernous nerve crush injury in the rat

Peripheral sensory diabetic neuropathy is characterized by morphological, electrophysiological and neurochemical changes to a subpopulation of primary afferent neurons. Here, we utilized a transgenic mouse model of diabetes (OVE26) and age-matched controls to histologically examine the effect of chronic hyperglycemia on the activity or abundance of the enzymes acid phosphatase, cytochrome oxidase and NADPH-diaphorase in primary sensory neuron perikarya and the dorsal horn of the spinal cord. Quantitative densitometric characterization of enzyme reaction product revealed significant differences between diabetic, compared to control, animals for all three enzymes. Levels of acid phosphatase reaction product were found to be significantly reduced in both small diameter primary sensory somata and the dorsal horn. Cytochrome oxidase activity was found to be significantly lower in small primary sensory somata while NADPH-diaphorase labeling was found to be significantly higher in small primary sensory somata and significantly lower in the dorsal horn. In addition to these observed biochemical changes, ratiometric analysis of the number of small versus large diameter primary sensory perikarya in diabetic and control animals demonstrated a quantifiable decrease in the number of small diameter cells in the spinal ganglia of diabetic mice. These results suggest that the OVE26 model of diabetes mellitus produces an identifiable disturbance in specific metabolic pathways of select cells in the sensory nervous system and that this dysfunction may reflect the progression of a demonstrated cell loss.     

Subcutaneous fat remodelling in Southeast Asian infants and children

Longitudinal data on 1,048 Thai children were evaluated for evidence of subcutaneous fat remodelling. Fat distribution, as defined by 100 (triceps/[triceps + subscapular]), was more pronounced in the limbs during infancy but shifted toward the trunk thereafter. Subsequent stepwise regression analysis indicated that biological age--as measured by Gruelich-Pyle bone age--and weight together explained between 0.8% and 14.5% of variance in fat distribution, with generally larger R2 values over age and for males. Relationships were curvilinear, with sex differences in slope. Path analysis supported the model that weight was a major causal agent primarily after infancy, whereas biological age had a small influence both in infancy and in late childhood. These findings indicate that trunk fat deposition is a normal feature of childhood. They also suggest that hypotheses which associate elevated trunk fatness with disorders of glucose metabolism are invalid for younger children.