Using Problem-based Learning to Explore Unseen Academic Potential

One goal of the US Department of Education-funded Project Insights was to see if the use of Problem-based Learning (PBL) would encourage students to reveal previously unseen academic potential. Two PBL units were taught to 271 sixth grade students in 13 classrooms. Afterwards, teachers identified students who demonstrated previously unseen academic potential during the PBL units. This advanced academic potential group was compared with students identified as gifted using district criteria and the remaining sixth grade students. Measures included standardized achievement test scores, teacher ratings of students’ engagement in PBL, and independent ratings of students’ performance on specific PBL assignments. Results of comparisons support the teacher’s identification of the advanced academic potential students as a group distinct from both from the traditionally identified students and general education students. Findings suggest that a well-designed, engaging curriculum such as PBL can create learning context that encourages more students to reveal academic potential

Myth 19: Is Advanced Placement an adequate program for gifted students

covered with myths and assumptions that it is hard to get a clear view of the issues. Let us find the answer about AP by looking at current realties. Reality: AP is hard for gifted students to avoid. AP affects class rank through weighted grades. AP course taking, AP test scores, and AP class grades are three of the top 10 college admissions criteria (Breland, Maxey, Gernand, Cumming, & Trapani, 2002; Espenshade, Hale and Chung, 2005). AP test scores of 4 or 5 can save time and money in college. Students know these realities: In 2008, 1.58 million teens took 2.74 million AP tests, including 264,480 ninth and tenth graders. More than 11,000 students took six or more AP exams (College Board, 2008). Reality: AP never was a program for gifted stu

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)