PubMed Health⌕ Search

PubMed · 16392691

Formulating secondary-level reading interventions.

Abstract

Recent advances concerning emerging/beginning reading skills, positive behavioral support (PBS), and three-tiered schoolwide prevention models combined with federal mandates (i.e., IDEA and No Child Left Behind) have stimulated interest in providing early and intensive instructional intervention services to children at risk for reading and behavior problems. New measures for identifying students as early as kindergarten who are not acquiring early basic literacy skills make this possible. However, questions regarding exactly how to formulate, deliver, sustain, and manage secondary-level interventions remain to be addressed. This paper describes first-year, first-grade findings for students participating in secondary-level interventions (i.e., small-group reading instruction) in a randomized trial of the efficacy of secondary and tertiary reading and behavior interventions under way at the Center for Early Intervention in Reading and Behavior, University of Kansas. The formulation of the experimental secondary-level intervention was guided by evidence supporting the efficacy of (a) small groups of 3 to 6 participating students and low student-teacher ratio combined with (b) explicit, phonics-based instruction. Selected curricula were Reading Mastery, Proactive Reading, Programmed Reading, and Read Well, use of which varied by choice across experimental-group schools. PBS was an additional intervention context in experimental schools. Comparison schools and first-grade teachers did not employ the three-tiered model, early screening, or PBS; most students were taught using conventional whole-group instruction, little or no individualization, and curricula with weak scientific evidence. Initial results indicate significantly larger growth for experimental secondary-level at-risk students than for comparisons. Experimental-group first graders not showing growth were those identified with disabilities or behavioral risks and English language learners. Implications are discussed.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Debra M Kamps, Charles R Greenwood. Formulating secondary-level reading interventions.. https://doi.org/10.1177/00222194050380060501

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Prevalence and risk factors for persistent faecal carriage of extended spectrum beta-lactamase producing Escherichia coli in a paediatric community population.

OBJECTIVE: To investigate clinical and microbiological factors associated with persistent faecal carriage of extended spectrum beta-lactamase (ESBL) producing Escherichia coli in infants. METHODS: Between 2010 and 2022, children aged 3 months to 2 years old were sampled in a community setting in France, at two visits, V1 and V2, 3-24 months apart, to screen for prolonged faecal carriage of ESBL-producing E. coli. Patient clinical information and whole genome sequence of each isolate were used for association studies. RESULTS: A total of 4641 children were sampled. 375 (8%) carried an ESBL-producing Enterobacterales, among which 142 of ESBL-producing E. coli carriers were once again sampled at V2 and included in this study. 21.8% (n = 31/142) and 18.4% (n = 16/99) carried the same ESBL-producing E. coli clone for at least 3 and 6 months, respectively. B2 phylogroup, and among which ST131 clones were associated with an increased risk of persistent carriage. Multivariate analysis identified virulence associated genes involved in adhesion (papC/papGII allele and a tia-like gene) and encoding toxin (senB) as major risk factors for persistence. A genome wide association study highlighted the potential role of the frz metabolic operon, known to be involved in enterocytes adhesion/internalisation. CONCLUSION: Main extraintestinal pathogenic E. coli genomic features (phylogenetic background, adhesion properties) are associated with ESBL-producing E. coli gut colonisation persistence in infants, which could potentially lead to an increased risk of febrile urinary tract infection in these patients.

Child↗

Extensive and differential platinum chemotherapy mutagenesis in livers of children.

Childhood cancer survivors often experience late adverse effects that may be linked to chemotherapy mutagenesis. We studied chemotherapy mutagenesis in normal pediatric tissues using duplex sequencing (NanoSeq) to enable the detection of mutations from single DNA molecules. We found that platinum chemotherapeutics increased the mutation burdens of normal pediatric tissues to levels seen in adults. In the liver, platinum agents imparted a tissue-specific mutational signature that was absent from other tissues. Gene-focused duplex sequencing revealed that chemotherapy mutagenesis generates a great diversity of nonsynonymous variants, some of which may have functional potential, such as leukemogenic variants in blood. Our findings demonstrate extensive chemotherapy mutagenesis in normal tissues of children, which may provide a plausible link between chemotherapy exposure and adverse effects in later life.

Child↗

Clinical and immunological characterization of a child with a homozygous TBK1 kinase-domain truncation.

TBK1 is a serine-tyrosine kinase protein that transmits signals from pattern recognition receptors to the NF-κB pathway leading to production of Type 1 Interferons. Mutations in this protein have been associated with arthritis, vasculitis, herpes simplex encephalitis and amyotrophic lateral sclerosis. In the current study, we characterized the functional consequences of a TBK1-variant bearing a truncation in exon 4 and 5 in a patient with poly arthritis resembling juvenile idiopathic arthritis and necrotizing encephalitis. The truncation was associated with reduced TBK1 protein abundance and altered phosphorylation. The variant was associated with increased basal/and or Poly-I: C induced IL-6, TNFα, IL-1β and IL-18 and type 1 Interferon ex vivo. Our findings expand the phenotypic spectrum of TBK1 loss-of-function variants and may provide insight into the management of immune dysregulation in affected patients.

Child↗