Project E3 (E-Filter, E-Frame, E-Page)

E-Filter: Our E-flow air filtration system is designed solely from ewaste materials. It uses solar e-wastes to generate power and purifies the air from smoke, odor, toxins & dust by passing it through several designed filters. E-page: Check our e-wasterecycling ideas website (http://e-waste-recycle-idea.blogspot.com/) Use these simple ideas to use your old electronics, enjoy creating your new stuff by yourself, feel green and share your new ideas with others. E-Frame: We designed an eframe; a digital photo frame which displays photographs and movies in high resolution with voice.Ope

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)

An appraisal of the computed axial tomographic appearance of the human mesentery based on mesenteric contiguity from the duodenojejunal flexure to the mesorectal level

OBJECTIVE: The human mesentery is now regarded as contiguous from the duodenojejunal (DJ) to anorectal level. This interpretation prompts re-appraisal of computed tomography (CT) images of the mesentery. METHODS: A digital model and reference atlas of the mesentery were generated using the full-colour data set of the Visible Human Project (VHP). Seventy one normal abdominal CT images were examined to identify mesenteric regions. CT appearances were correlated with cadaveric and histological appearances at corresponding levels. RESULTS: Ascending, descending and sigmoid mesocolons were identifiable in 75%, 86% and 88% of the CTs, respectively. Flexural contiguity was evident in 66%, 68%, 71% and 80% for the ileocaecal, hepatic, splenic and rectosigmoid flexures, respectively. A posterior mesocolic boundary corresponding to the anterior renal fascia was evident in 40% and 54% of cases on the right and left, respectively. The anterior pararenal space (in front of the boundary) corresponded to the mesocolon. CONCLUSIONS: Using the VHP, a mesenteric digital model and reference atlas were developed. This enabled re-appraisal of CT images of the mesentery, in which contiguous flexural and non-flexural mesenteric regions were repeatedly identifiable. The anterior pararenal space corresponded to the mesocolon. KEY POINTS: The Visible Human Project (VHP) allows direct identification of mesenteric structures. Correlating CT and VHP allows identification of flexural and non-flexural mesenteric components. Radiologic appearance of intraperitoneal structures is assessed, starting from a mesenteric platform