Mobile Computing for Trauma and Surgical Care Continuous Education

In medical domain, mobile computing has proven to be convenient, effective, and productive. With varying screen sizes, there is a challenge to present the right information in the right format such that medical practitioners can access information quickly. In this thesis, we discuss how mobile computing can be used as a way of continuous education for medical practitioners in the field of trauma and surgical care, and provide design guidelines on how to effectively present information on different mobile form factors. The focus is on three screen sizes- 4.7, 7 and 10.1 in., and three interaction methods - dropdown, slide, and tab menu. Results indicate that medical practitioners preferred 7 in. device that enabled them to have information at a glance and aid them in surgical decision making. In addition, the tab menu was the most convenient, intuitive and attractive out of the three interaction methods

تصور مقترح لحوكمة الأنشطة اللاصفية بمدارس التعليم العام بالمملكة العربية السعودية في ضوء التجارب العالمية

الأهداف: سعت الدراسة التعرف إلى واقع حوكمة الأنشطة اللاصفية بمدارس التعليم العام بالمملكة العربية السعودية، وبناء تصوُّر مقترح للحوكمة في ضوء التجارب العالمية. المنهجية: اعتمدت الدراسة المنهج الوصفي الوثائقي، واستخدمت أداة تحليل المحتوى لجمع وتحليل البيانات النوعية من عينة متمثلة بعدد (23) وثيقة رسمية بالدول الخمس المرجعية. كما تم استخدام آلية تحليل محتوى الوثائق بطريقته الاستنباطية (العساف، 2012)، والتي تسمح بمقارنة نتائج التحليل بين الوثائق في الدول المرجعية، وبالتالي استنتاج واستخراج ما يجيب عن تساؤلات الدراسة في مجالات الدراسة القياسية (السياسات واللوائح المنظمة للأنشطة اللاصفية، آليات تعزيز مشاركة الطلبة، التمويل وضوابط مشاركة القطاعات). النتائج: توصلت الدراسة في نتائجها إلى اتفاق المملكة مع الممارسات العالمية في مدارس التعليم العام في كل من: (توفير دليل تنظيمي للأنشطة اللاصفية، تحديد مسؤوليات العاملين المشرفين على الأنشطة اللاصفية، تقديم الأنشطة اللاصفية في الفترة الصباحية والمسائية، تمويل ودعم الأنشطة اللاصفية عبر الشراكة مع القطاع الخاص، وإعطاء مدير المدرسة صلاحية الاتفاق مع القطاع الخاص). في حين لا توجد معايير خاصة لاختيار المشاركين المحتملين من القطاع الخاص في تنفيذ الأنشطة اللاصفية في المملكة، إلى جانب وجود فجوة بين المملكة والممارسات العالمية في تنويع طرائق وأساليب تحفيز الطلبة للمشاركة في الأنشطة اللاصفية، وتوظيف وسائل الإعلام في التعريف بالأنشطة اللاصفية والمدارس المتميزة، وربط المشاركة في الأنشطة اللاصفية بالقبول في الجامعات. الخلاصة: توصلت الدراسة إلى بناء تصوُّر مقترح لبناء السياسات واللوائح المنظمة للأنشطة اللاصفية بمدارس التعليم العام بالمملكة العربية السعودية في ضوء التجارب العالمية، بالإضافة إلى بناء الأدلة الإجرائية لحوكمتها

Role of GSα-dependent signaling in bone homeostasis, condylar remodeling and enamel mineralization

The Dentin Matrix Protein (DMP1) is a critical regulator of bone and dentin mineralization and this protein is highly expressed in osteocytes and odontoblasts. Gs alpha (Gsα) protein, the main intracellular signal of a broad class of G-protein coupled receptors (GPCRs), is highly expressed in bone cells, including osteocytes. We and others have demonstrated that mice lacking the Gsα expression, predominantly in osteocytes (DMP1-GsαKO mice), develop severe osteopenia driven by a marked reduction in osteoblast activity associated with a significant increase in SOST/sclerostin expression. In this study, we have examined the role of Gsα in the jaws and teeth of DMP1-GsαKO mice to investigate if the absence of Gsα expression in osteocytes and odontoblasts altered teeth and jaws morphology. Our previous studies showed that DMP1-GsαKO leads to a significant decrease in both trabecular and cortical bone content in the skeleton, as assessed by μCT and histomorphometric analysis. Here we characterize the dental and craniofacial phenotype of DMP1-GsαKO mice. Results showed that DMP1-GsαKO had decreased total mandibular bone mineral density (BMD), total mandibular mineral content (BMC), condylar BMD and total tooth mineralization as assessed by DEXA using a Lunar PIXImus II densitometer. Furthermore, μCT analysis revealed that condylar bone volume and tooth mineralization is reduced in DMP1-GsαKO mice compared to control littermate. μCT also showed that the overall skull size and specifically the zygomatic bone is larger in the control group. Next, we examined H&E histological sections of the jaws of DMP1-GsαKO and control mice, which confirmed the osteopenic phenotype. Tartrate-resistant acid phosphatase (TRAP) staining showed that the number of TRAP-positive osteoclasts was increased in the DMP1-GsαKO mice compared to controls, suggesting increased bone resorption. In conclusion, our studies identified Gsa signaling in osteocytes and odontoblasts as important in maintaining normal bone and tooth homeostasis

FPGA Realizations of Walsh Transforms for Different Transform and Word lengths into Xilinx and Altera Chips

This paper presents FPGA realizations of Walsh transforms. The realizations are targetted for the system of arbitrary waveform generation, addition/ subtraction, multiplication, and processing of several signals based on Walsh transforms which is defined in term products of Rademacher functions. Input signals are passing through the system in serial, the output either signals or coefficients are also passing out in serial. To minimize the area utilization when the systems are realized in FPGA chips, the word lengths of every processing step have been designed carefully. Based on this, FPGA realizations of those various applications into Xilinx and Altera chips have been done. In Xilinx realizations, Xilinx ISE was used to display the results and to extract some critical parameters such as speed and static power. Meanwhile, the realizations into Altera chips have been conducted using Quartus. Comparisons of speed and power among Xilinx and Altera chip realizations are presented here even though this is not an apple to apple comparison. Finally, it can be concluded that Walsh transforms can be realized not only for the applications that have been done here, but it is potential can be used for other applications

FPGA Hardware Realization: Addition of Two Digital Signals Based on Walsh Transforms

This paper presents hardware realization of addition of two digital signals based on Walsh transforms and inverse Walsh transforms targeted to the Xilinx FPGA Spartan 3 board. The realization utilizes Walsh Transform to convert the input data to frequency domain and the inverse Walsh transform to reconvert the data from frequency domain. The designed system is capable of performing addition, subtraction, multiplication and Arbitrary Waveform Generation (AWG). However, in the present work, the hardware realization of addition only has been demonstrated. The Clock frequency for realization into the board is supplied by an external function generator. Output results are captured using a logic analyzer. Input data to the board (system) is passed manually through the available slide switches on-board

Design of Real Time Walsh Transform for Processing of Multiple Digital Signals

This paper presents the design and implementation of multiple digital signals processing using real-time Walsh transforms. The design of real time Walsh transform is done in such a way that it starts producing outputs instantly even before all input data have entered the system. The system consists of Walsh Transform circuit, several Digital Signal Processing (DSP) circuits, and an inverse Walsh transform circuit. The real time Walsh and inverse Walsh transforms are also designed to produce right results for any possible combinations of input data. DSP blocks are able to perform addition, subtraction, and dyadic convolution process of Walsh coefficients of more than one digital signals. Comparisons to the previous methods are briefly presented. It was found that the design of real time Walsh transform structure has better performance than many of the previously reported results in the literature.DOI:http://dx.doi.org/10.11591/ijece.v3i2.196

Identification of new targets for the treatment of head and neck cancer: N-glycosylation gene DPAGT1 and β-catenin/CBP signaling

Head and neck squamous cell carcinoma (HNSCC) is pernicious disease with majority of cases presenting as oral squamous cell carcinoma (OSCC). OSCC is characterized by tumor heterogeneity, locoregional metastases and resistance to existing treatments. OSCC five-year overall survival rates are currently ~ 50 % with few therapeutic options available. Cancers are typically associated with dysregulated signaling pathways that normally have vital roles in embryonic development and hemostasis. We have focused on two homeostatic pathways, protein N-glycosylation and the canonical Wnt/β-catenin signaling, which have been shown to converge on each other’s activities. These pathways, when left unchecked, drive early pathogenesis and/or metastasis of a range of cancers, including OSCC. Aberrant activation of the DPAGT1 gene, encoding a key regulatory enzyme that functions at the first committed step in the protein N-glycosylation pathway, has been shown to be associated with OSCC. In OSCC, high DPAGT1 expression drives hyper-glycosylation of E-cadherin and loss of intercellular adhesion. Here, we provide evidence that ectopic expression of DPAGT1 in indolent OSCC CAL27 cells induced epithelial-to-mesenchymal transition (EMT) by upregulation of a key transcription factor, ZEB1, and mesenchymal protein, vimentin, coincident with increased cell migration. In contrast, partial knockdown of DPAGT1 in metastatic OSCC HSC-3 cells reduced expression of the EMT markers, diminished cell migration and enhanced intercellular adhesion. Further, inhibition of the DPAGT1 enzyme, GPT, with tunicamycin interfered with orthotopic tongue tumor growth and metastasis in nude mice coincident with diminished expression of vimentin- positive cells invading the tongue stroma. One mechanism responsible for increased DPAGT1 expression in OSCC is transcriptional activation by β-catenin. We now show that blocking transcriptional activity of β-catenin by interfering with its interaction with the cAMP-responsive element binding (CREB)-binding protein (CBP) using a small molecule inhibitor, ICG-001, inhibited cell proliferation and mesenchymal cell phenotypes in cellular models. In addition, ICG-001 abrogated tumor growth and metastases in zebrafish and murine models. Microarray analyses of ICG-001 gene expression signature revealed inhibition of genes involved in cell proliferation, survival, stemness, as well as N-glycosylation, but upregulation of genes functioning in cell adhesion and cell polarity. Importantly, the ICG-001 inhibition-associated transcriptional signature tracked with advanced tumor grade and poor survival in human patients. Our studies provide the first evidence that aberrant activation of DPAGT1 and β-catenin signaling promotes aggressive traits of OSCC cells and suggest that targeting the β-catenin/CBP interaction in the nucleus may provide an effective novel strategy for OSCC therapy

Abstract 803: Targeting β-catenin/CBP signaling in OSCC

OBJECTIVES: Oral squamous cell carcinoma (OSCC) is an aggressive malignancy characterized by molecular heterogeneity and locoregional spread associated with high morbidity. Aggressive cancers are thought to arise from populations of cancer initiating cells (CICs) that exhibit the properties of stem cells and drive tumor development, recurrence and resistance to therapy. The transcriptional regulator, β-catenin, has been implicated in OSCC CICs. Nuclear β-catenin has been shown to recruit the chromatin remodeling CREB binding protein (CBP) to drive expression of proliferation and survival genes, as well as genes that maintain stem-like phenotypes. We hypothesized that targeting β-catenin-CBP interaction will inhibit CICs in oral tumors and restore an epithelial phenotype. METHODS: To test tumor aggressive potential of OSCC CICs, we used zebrafish as a model system. We isolated CD44+CD24hiCD29hi cells fom aggressive HSC-3 OSCC cells by FACS and assayed their ability to drive tumor growth and metastases in zebrafish compared to unsorted and CD44+CD24lowCD29low cells. In addition, we examined the role of the β-catenin/CBP axis in the aggressive phenotype of these cells. We also assessed whether the β-catenin/CBP axis affected CICs in tumors from immune competent HPV+ mice. RESULTS: Zebrafish injected with subpopulation of cells co-expressing CD44+CD24hiCD2hi primitive cell surface markers drove rapid tumor growth and metastases, followed by unsorted and sorted CD44+CD24lowCD29low. Treatment of CD44+CD24hiCD29hi cells with a small molecule inhibitor of the β-catenin-CBP interaction, ICG-001, interfered with tumor growth and metastases in zebrafish. Further, ICG-001 inhibited tumor growth in immunocompetent HPV+ murine model. On a cellular level, ICG-001 promoted membrane localization of β-catenin, enhanced E-cadherin adhesion and restored epithelial phenotype. Significantly, ICG-001 gene signatures tracked with reduced overall patient survival in the cancer genome atlas, TCGA. Conclusion: Our studies indicate that the β-catenin/CBP axis promotes OSCC CICs and that ICG-001 may be an effective therapeutic agent for this malignancy.Support: Evans Center for Interdisciplinary Biomedical Research ARC funding AU 5303015 8000000