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Purpose: The aim of this study is to determine if prospective determinations of citrulline could be predictive of the bowel adaptation in children with short bowel syndrome (SBS)., Methods: Between March 2005 and March 2010, we prospectively included 28 SBS patients on parenteral nutrition. The citrulline and the enteral intake determinations were scheduled at the inclusion and at 6-month intervals. We assessed the correlation between citrulline and bowel length as well as enteral caloric intake, longitudinal trend of citrulline and association between patients characteristics according to the course of bowel adaptation., Results: Citrulline significantly correlated with the residual duodenum-jejunum length (r (2) = 0.22, P = 0.0113) and with enteral intake (r (2) = 0.20, P = 0.016 and r (2) = 0.48, P = 0.0001). Baseline citrulline at the cutoff >10 μmol/L and a longitudinal increase >25% provided a weak association with bowel adaptation (likelihood ratio (LR), 2.6 and 2.4, respectively), unlike residual small bowel length ≥20 cm and the presence of >50% of the colon (LR, 10 and 6, respectively)., Conclusions: Citrulline seems to be a powerful biomarker of the intestinal function, showed by the correlation with the residual duodenum-jejunum length and the enteral absorption, but not of its prospective changes during the bowel adaptation process. Future studies may be necessary to confirm this finding.

Recent experiments have characterized the dependence of saccade gain adaptation on the characteristics of the visual error following inaccurate saccades. We currently know little about the potential role of non-visual information in driving saccade adaptation. The brain could use non-visual signals from the saccade burst generator or extraocular muscle (EOM) proprioceptors to determine if the eye had rotated the appropriate distance to aim at a target. Both saccade-related burst signals and EOM proprioceptive information reach the posterior vermis of the cerebellum, a brain area strongly implicated in saccade adaptation. In the experiment described here we determined if non-visual information has a significant affect on saccade adaptation. We made monkey saccades hypometric with intra-saccade target movements and then tested the recovery of saccade gain toward normal under three conditions: (1) when the target was continuously visible, (2) when the target extinguished for 1000 ms beginning during the saccade, and (3) when the monkey remained in the dark. In the first condition both visual and non-visual indications of hypometria were available. In the second, only non-visual information was available. In the third, the monkey made no visually guided saccades and very few spontaneous saccades in the dark so neither visual nor non-visual information could drive adaptation. We found that, though it was hypometric, saccade size during recovery changed the same small amount when monkeys made saccades to extinguishing targets or remained in the dark. Saccade size changed significantly (approximately 5x) more during recovery when the monkey tracked continuously visible targets. Thus non-visual information has no influence on adaptation and visual post-saccade error is the only known driver of saccade adaptation., (Copyright 2002 Elsevier Science B.V.)

Saccade accuracy is fundamental to clear vision. The brain maintains saccade accuracy by altering commands for saccades that are consistently inaccurate. For example, saccades that consistently overshoot their targets gradually become smaller. The signal that drives the adaptation of saccade size is not well understood. Previous reports propose that corrective movements and visual errors, both generated after inaccurate saccades, could be responsible for a change in saccade size. Here we show that we can elicit normal reductions in saccade size while eliciting few or no correction saccades. These normal reductions in saccade size indicate that visual errors, not correction saccades, drive the adaptation of saccades.

Saccadic gain (saccade amplitude/target amplitude) can be reduced gradually by repeatedly stepping the target backward during the saccade. The gain reduction produced by this paradigm is thought to be driven by an error signal created by the backstep. We investigated the effects of varying the timing of this error signal relative to the end of the saccade by using two different paradigms in macaques. In the brief backstep paradigm, the target was stepped backward 30% during the saccade but extinguished after different durations. For very short backstep durations (32 ms), little gain reduction occurred. As backstep duration increased, the amount of gain reduction also increased. When backstep duration reached 80 ms, the amount of gain reduction was just under that achieved during the conventional adaptation paradigm in which the backstep remained visible for 1000-1200 ms. In the delayed backstep paradigm, as the saccade occurred, we extinguished the target and then, after a delay, illuminated it for 1 s at the backstep location. In most experiments with short delay times of 16-64 ms, the saccadic gain reduction reached that achieved during conventional adaptation. At delays of 112-208 ms, the amount of gain reduction decreased to approximately 75% of that reached during conventional adaptation. With still longer delays, the amount of gain reduction decreased more gradually. At delays of 750 ms, average gain reduction was 10%. By delays of 1.5 s, gain reduction had fallen essentially to zero. Taken together, these data suggest that the error signal must be present for a limited time ( approximately 80-100 ms) after the saccade to produce the most robust saccadic gain adaptation. However, errors present as long as 750 ms after the saccade still can produce a significant gain reduction.

The brain maintains saccade accuracy by modifying saccades that are consistently inaccurate (e.g. hypermetric). To determine whether this adaptation is influenced by the visual background we used several different target and background movements to elicit changes in saccade gain. In almost all cases, the target spot drove gain changes. The background had no effect on, or slightly reduced, adaptation. We conclude that the saccade adaptation mechanism is driven almost entirely by stimuli on or near the fovea and is affected very little by visual stimuli falling more peripherally.

The gain of saccadic eye movements can be altered gradually by moving targets either forward or backward during targeting saccades. If the gain of saccades to targets of only one size is adapted, the gain change generalizes or transfers only to saccades with similar vectors. In this study, we examined the spatial extent of such saccadic size adaptation, i.e., the gain adaptation field. We also attempted to adapt saccade direction by moving the target orthogonally during the targeting saccade to document the extent of a direction or cross-axis adaptation field. After adaptive gain decreases of horizontal saccades to 15 degrees target steps, >82% of the gain reduction transferred to saccades to 25 degrees horizontal target steps but only approximately 30% transferred to saccades to 5 degrees steps. For the horizontal component of oblique saccades to target steps with 15 degrees horizontal components and 10 degrees upward or downward vertical components, the transfer was similar at 51 and 60%, respectively. Thus the gain decrease adaptation field was quite asymmetric in the horizontal dimension but symmetric in the vertical dimension. Although gain increase adaptation produced a smaller gain change (13% increase for a 30% forward adapting target step) than did gain decrease adaptation (20% decrease for a 30% backward adapting target step), the spatial extent of gain transfer was quite similar. In particular, the gain increase adaptation field displayed asymmetry in the horizontal dimension (58% transfer to 25 degrees saccades but only 32% transfer to 5 degrees saccades) and symmetry in the vertical direction (50% transfer to the horizontal component of 10 degrees upward and 40% transfer to 10 degrees downward oblique saccades). When a 5 degrees vertical target movement was made to occur during a saccade to a horizontal 10 degrees target step, a vertical component gradually appeared in saccades to horizontal targets. More than 88% of the cross-axis change in the vertical component produced in 10 degrees saccades transferred to 20 degrees saccades but only 12% transferred to 4 degrees saccades. The transfer was similar to the vertical component of oblique saccades to target steps with either 10 degrees upward (46%) or 10 degrees downward (46%) vertical components. Therefore both gain and cross-axis adaptation fields have similar spatial profiles. These profiles resemble those of movement fields of neurons in the frontal eye fields and superior colliculus. How those structures might participate in the adaptation process is considered in the DISCUSSION.