Treating Pediatric Feeding Disorders and Dysphagia: Evidence-Based Interventions for School-Based Clinicians.

PURPOSE: Children with pediatric feeding disorder (PFD) and dysphagia are increasingly prevalent in school-based caseloads. This tutorial discusses the current best practices for treating children with PFD and dysphagia as well as considerations for service delivery in educational settings. METHOD: The rationale for treating PFD and dysphagia in an educational setting is discussed. A review of various interventions for PFD and dysphagia and a discussion of the available evidence are provided. The principles of experience-dependent neuroplasticity and theory-driven practice are discussed in light of the need for additional empirical research. Practical considerations to enhance evidence-based practice for PFD and dysphagia in educational settings are explored. RESULTS: The reader will be able to identify evidence-based interventions for students with PFD and dysphagia and plan for the implementation of these approaches in the school setting. CONCLUSIONS: Students with PFD and dysphagia require skilled interventions to support their participation in educationally relevant activities and to promote continued development of feeding and swallowing skills while at school. A discussion of the current evidence for various interventions is provided to promote the utilization of evidence-based interventions in school-based settings.

Identifying allelic loss and homozygous deletions in pancreatic cancer without matched normals using high-density single-nucleotide polymorphism arrays.

Recent advances in oligonucleotide arrays and whole-genome complexity reduction data analysis now permit the evaluation of tens of thousands of single-nucleotide polymorphisms simultaneously for a genome-wide analysis of allelic status. Using these arrays, we created high-resolution allelotype maps of 26 pancreatic cancer cell lines. The areas of heterozygosity implicitly served to reveal regions of allelic loss. The array-derived maps were verified by a panel of 317 microsatellite markers used in a subset of seven samples, showing a 97.1% concordance between heterozygous calls. Three matched tumor/normal pairs were used to estimate the false-negative and potential false-positive rates for identifying loss of heterozygosity: 3.6 regions (average minimal region of loss, 720,228 bp) and 2.3 regions (average heterozygous gap distance, 4,434,994 bp) per genome, respectively. Genomic fractional allelic loss calculations showed that cumulative levels of allelic loss ranged widely from 17.1% to 79.9% of the haploid genome length. Regional increases in "NoCall" frequencies combined with copy number loss estimates were used to identify 41 homozygous deletions (19 first reports), implicating an additional 13 regions disrupted in pancreatic cancer. Unexpectedly, 23 of these occurred in just two lines (BxPc3 and MiaPaCa2), suggesting the existence of at least two subclasses of chromosomal instability (CIN) patterns, distinguished here by allelic loss and copy number changes (original CIN) and those also highly enriched in the genomic "holes" of homozygous deletions (holey CIN). This study provides previously unavailable high-resolution allelotype and deletion breakpoint maps in widely shared pancreatic cancer cell lines and effectively eliminates the need for matched normal tissue to define informative loci.