What Works in Collaboration? Identifying Key Ingredients to Improve Service Delivery in Schools.

Purpose: This survey study examined factors that may influence interprofessional collaboration in schools to support children with oral and written language impairments, namely, knowledge, collaborative beliefs and practices, and resources.

Method: A survey was conducted across 319 school-based professionals, in a partnering public school district, to examine these constructs within the context of each individual participant's professional role.

Results: Between-groups comparisons were made between special educators, general educators, paraprofessionals, and indirect educators (i.

Abnormal prostaglandin E2 production blocks myogenic differentiation in myotonic dystrophy.

The congenital form of myotonic dystrophy type 1 (DM1) is the most severe type of the disease associated with CTG expansions over 1500 repeats and delayed muscle maturation. The mechanistic basis of the congenital form of DM1 is mostly unknown. Here, we show that muscle satellite cells bearing large CTG expansions (>3000) secrete a soluble factor that inhibits the fusion of normal myoblasts in culture.

Absence of a differentiation defect in muscle satellite cells from DM2 patients.

Myotonic dystrophy type 1 (DM1) and type II (DM2) are dominantly inherited multisystemic disorders. DM1 is triggered by the pathological expansion of a (CTG)(n) triplet repeat in the DMPK gene, whereas a (CCTG)(n) tetranucleotide repeat expansion in the ZNF9 gene causes DM2. Both forms of the disease share several features, even though the causative mutations and the loci involved differ.

RNA based gene therapy for dominantly inherited diseases.

There are numerous examples in the literature of gene therapy applications for recessive disorders. There are precious few instances, however, of studies conducted to treat dominantly inherited pathologies. The reasons are simple: there are fewer cases of dominantly inherited diseases on one hand, but mostly it is far easier to correct recessive mutations than dominant ones.

Mechanistic features of CAG*CTG repeat contractions in cultured cells revealed by a novel genetic assay.

Trinucleotide repeats (TNRs) undergo high frequency mutagenesis to cause at least 15 neurodegenerative diseases. To understand better the molecular mechanisms of TNR instability in cultured cells, a new genetic assay was created using a shuttle vector. The shuttle vector contains a promoter-TNR-reporter gene construct whose expression is dependent on TNR length.

Replication and expansion of trinucleotide repeats in yeast.

The mechanisms of trinucleotide repeat expansions, underlying more than a dozen hereditary neurological disorders, are yet to be understood. Here we looked at the replication of (CGG)(n) x (CCG)(n) and (CAG)(n) x (CTG)(n) repeats and their propensity to expand in Saccharomyces cerevisiae. Using electrophoretic analysis of replication intermediates, we found that (CGG)(n) x (CCG)(n) repeats significantly attenuate replication fork progression.