Maximizing Educator Enhancement: Aligned Seminar And Online Professional Development

Professional development and learning has a long history in seminar-like models, as well as in the more educator-personal delivery approaches.  The question is whether an intentionally coordinated, integrated combination of the two PDL approaches will have best impacts for educators as quantified in improved student performance.  Contrasts between baseline and Post-Program performance levels showed 19% gains in Reading and 24% gains in Math, significantly beyond expectation.  Analyses for Title 1 schools showed significant shrinkage of performance gaps with contrasted non-Title 1 schools.  These gains outpaced those found for either PDL approach alone, indicating that educational leaders will be wise to undertake implementation of intentionally aligned and coordinated approaches combining PDL Seminars with online, on-demand PDL.

From Burdens To Benefits: The Societal Impact Of PDL-Enriched, Efficacy-Enhanced Educators

Societies continue to absorb increased burdens in cost for helping citizens unable to achieve at optimal levels.  Building on past research, we project educational benefits to offset current societal burdens through enhanced educator capabilities.  Studies reviewed show participation in a high-impact professional development and learning solution resulted in improved student performance and reduced dropout rates, reduced disciplinary rates and increased rates for college-bound, along with lower teacher turnover.  Computations show that generalization of such impacts should trade societal burdens for benefits at between $3.7 billion and$6.9 billion within the first year.  Cumulatively within 20 years the burdens converted to benefits are projected to exceed $85 billion.  Enhanced educator capabilities will substantively reduce needs and costs for societal programs, replaced with tangible benefits to all

Palindromic GOLGA8 core duplicons promote chromosome 15q13.3 microdeletion and evolutionary instability.

Recurrent deletions of chromosome 15q13.3 associate with intellectual disability, schizophrenia, autism and epilepsy. To gain insight into the instability of this region, we sequenced it in affected individuals, normal individuals and nonhuman primates. We discovered five structural configurations of the human chromosome 15q13.3 region ranging in size from 2 to 3 Mb. These configurations arose recently (∼0.5-0.9 million years ago) as a result of human-specific expansions of segmental duplications and two independent inversion events. All inversion breakpoints map near GOLGA8 core duplicons-a ∼14-kb primate-specific chromosome 15 repeat that became organized into larger palindromic structures. GOLGA8-flanked palindromes also demarcate the breakpoints of recurrent 15q13.3 microdeletions, the expansion of chromosome 15 segmental duplications in the human lineage and independent structural changes in apes. The significant clustering (P = 0.002) of breakpoints provides mechanistic evidence for the role of this core duplicon and its palindromic architecture in promoting the evolutionary and disease-related instability of chromosome 15

Palindromic GOLGA8 core duplicons promote chromosome 15q13.3 microdeletion and evolutionary instability

Recurrent deletions of chromosome 15q13.3 associate with intellectual disability, schizophrenia, autism and epilepsy. To gain insight into the instability of this region, we sequenced it in affected individuals, normal individuals and nonhuman primates. We discovered five structural configurations of the human chromosome 15q13.3 region ranging in size from 2 to 3 Mb. These configurations arose recently (∼0.5-0.9 million years ago) as a result of human-specific expansions of segmental duplications and two independent inversion events. All inversion breakpoints map near GOLGA8 core duplicons-a ∼14-kb primate-specific chromosome 15 repeat that became organized into larger palindromic structures. GOLGA8-flanked palindromes also demarcate the breakpoints of recurrent 15q13.3 microdeletions, the expansion of chromosome 15 segmental duplications in the human lineage and independent structural changes in apes. The significant clustering (P = 0.002) of breakpoints provides mechanistic evidence for the role of this core duplicon and its palindromic architecture in promoting the evolutionary and disease-related instability of chromosome 15