Real-time analysis of large-scale neuronal imaging enables closed-loop investigation of neural dynamics.

Large-scale imaging of neuronal activities is crucial for understanding brain functions. However, it is challenging to analyze large-scale imaging data in real time, preventing closed-loop investigation of neural circuitry. Here we develop a real-time analysis system with a field programmable gate array-graphics processing unit design for an up to 500-megabyte-per-second image stream. Adapted to whole-brain imaging of awake larval zebrafish, the system timely extracts activity from up to 100,000 neurons and enables closed-loop perturbations of neural dynamics.

Ontogeny and prenatal expression of trefoil factor 3/ITF in the human intestine.

BACKGROUND: Trefoil factor 3 (TFF3) or intestinal trefoil factor (ITF), a peptide normally expressed and secreted by goblet cells at the mucosal surface of the small intestine and colon, is important for the maintenance and repair of the intestinal mucosal barrier. AIM: To study the ontogeny and developmental expression of TFF3 in human intestine. SUBJECTS: We examined TFF3 expression in formalin-fixed and paraffin-embedded intestinal tissues from 24 fetuses (gestational age [GA] 12-23 weeks) and 5 adults by immunohistochemical staining. To determine whether TFF3 is excreted into the fetal intestinal tract, first-passed meconium samples were collected from 43 newborn infants (gestational age 24-41 weeks). The presence of TFF3 was examined by Western blot analysis and the relative levels of TFF3 in the meconium were quantified with a slot blot assay. RESULTS: TFF3 can be detected by immunohistochemistry in human intestine as early as 12 weeks gestation. TFF3 is present in the meconium of newborn infants; no significant difference exists in TFF3 levels in the meconium of premature infants with birth weight (BW) less than 1500 g compared to those with birth weight equal to or more than 1500 g. CONCLUSION: Premature infant's susceptibility to intestinal mucosal injury is unlikely to be explained by developmental expression of TFF3 in human intestine since secreted TFF3 is not deficient in premature infants.

Chronic nicotine administration differentially alters jejunal and colonic inflammation in interleukin-10 deficient mice.

BACKGROUND: Cigarette smoking alters the course of inflammatory bowel disease, is associated with protection against ulcerative colitis, but aggravates or has no effect on Crohn's disease. While the aetiology of this discrepancy remains unclear, differences between location of involvement in ulcerative colitis and Crohn's disease have not been examined in these studies. AIM: To examine the effects of nicotine administration on the course of jejunitis and colitis in interleukin-10 deficient mice. METHODS: Male C57/BL10 IL-10 -/- and wild type mice were given nicotine (12.5 microg/ml) in their drinking water at age 12-14 weeks when they had developed clinical signs of inflammatory bowel disease. Gender and age matched control mice received tap water alone. All mice were killed after 2 weeks of treatment. Whole tissue sections of jejunum, proximal and distal colon were separated and examined by macroscopic and histological score. Northern blots were examined for somatostatin, intestinal trefoil factor and mucin-2. RESULTS: At 14-16 weeks, when the mice were killed, IL-10 -/- untreated control mice developed jejunitis (macroscopic score 1.4 +/- 0.5, microscopic score 2.0 +/- 0.2) and colitis (2.0 +/- 0.2 and 5.9 +/- 0.9, respectively). IL-10 -/- mice treated for 2 weeks with nicotine had significantly reduced colonic scores (1.4 +/- 0.6 and 2.2 +/- 0.15, respectively). In contrast, the jejunum was more severely damaged (2.6 +/- 0.4 and 4.0 +/- 0.3; P = 0.01, respectively). Nicotine significantly increased both somatostatin and intestinal trefoil factor mRNA expression in the colon but not in the jejunum; no effect was noted on mucin-2 or beta-actin mRNA expression. CONCLUSIONS: (1) Two weeks of nicotine administration leads to contrasting effects on jejunal and colonic inflammation in IL-10 -/- mice. (2) Nicotine ameliorated inflammation in the colon, which was associated with enhanced expression of two protective peptides.