Design of a Three-Dimensional Cognitive Mapping Approach to Support Inquiry Learning

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Improving the learning of clinical reasoning through computer-based cognitive representation

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Improving the learning of clinical reasoning through computer-based cognitive representation

Objective: Clinical reasoning is usually taught using a problem-solving approach, which is widely adopted in medical education. However, learning through problem solving is difficult as a result of the contextualization and dynamic aspects of actual problems. Moreover, knowledge acquired from problem-solving practice tends to be inert and fragmented. This study proposed a computer-based cognitive representation approach that externalizes and facilitates the complex processes in learning clinical reasoning. The approach is operationalized in a computer-based cognitive representation tool that involves argument mapping to externalize the problem-solving process and concept mapping to reveal the knowledge constructed from the problems. Methods: Twenty-nine Year 3 or higher students from a medical school in east China participated in the study. Participants used the proposed approach implemented in an e-learning system to complete four learning cases in 4 weeks on an individual basis. For each case, students interacted with the problem to capture critical data, generate and justify hypotheses, make a diagnosis, recall relevant knowledge, and update their conceptual understanding of the problem domain. Meanwhile, students used the computer-based cognitive representation tool to articulate and represent the key elements and their interactions in the learning process. Results: A significant improvement was found in students’ learning products from the beginning to the end of the study, consistent with students’ report of close-to-moderate progress in developing problem-solving and knowledge-construction abilities. No significant differences were found between the pretest and posttest scores with the 4-week period. The cognitive representation approach was found to provide more formative assessment. Conclusions: The computer-based cognitive representation approach improved the learning of clinical reasoning in both problem solving and knowledge construction

Description of a clinical decision support tool with integrated dose calculator for paediatrics

Medication errors, especially dosing errors are a leading cause of preventable harm in paediatric patients. The paediatric patient population is particularly vulnerable to dosing errors due to immaturity of metabolising organs and developmental changes. Moreover, the lack of clinical trial data or suitable drug forms, and the need for weight-based dosing, does not simplify drug dosing in paediatric or neonatal patients. Consequently, paediatric pharmacotherapy often requires unlicensed and off-label use including manipulation of adult dosage forms. In practice, this results in the need to calculate individual dosages which in turn increases the likelihood of dosing errors. In the age of digitalisation, clinical decision support (CDS) tools can support healthcare professionals in their daily work. CDS tools are currently amongst the gold standards in reducing preventable errors. In this publication, we describe the development and core functionalities of the CDS tool PEDeDose, a Class IIa medical device software certified according to the European Medical Device Regulation. The CDS tool provides a drug dosing formulary with an integrated calculator to determine individual dosages for paediatric, neonatal, and preterm patients. Even a technical interface is part of the CDS tool to facilitate integration into primary systems. This enables the support of the paediatrician directly during the prescribing process without changing the user interface. Conclusion: PEDeDose is a state-of-the-art CDS tool for individualised paediatric drug dosing that includes a certified calculator

Magnetic toys: forbidden for pediatric patients with certain programmable shunt valves?

Background: Inadvertent adjustments and malfunctions of programmable valves have been reported in cases in which patients have encountered powerful electromagnetic fields such as those involved in magnetic resonance imaging, but the potential effects of magnetic toys on programmable valves are not well known. Materials and methods: The magnetic properties of nine toy magnets were examined. To calculate the effect of a single magnet over a distance, the magnetic flux density was directly measured using a calibrated Hall probe at seven different positions between 0 and 120mm from the magnet. Strata II small (Medtronic Inc.), Codman Hakim (Codman & Shurtleff), and Polaris (Sophysa) programmable valves were then tested to determine the effects of the toy magnets on each valve type. Results: The maximal flux density of different magnetic toys differed between 17 and 540mT, inversely proportional to the distance between toy and measurement instrument. Alterations to Strata and Codman valve settings could be effected with all the magnetic toys. The distances that still led to an alteration of the valve settings differed from 10 to 50mm (Strata), compared with 5 to 30mm (Codman). Valve settings of Polaris could not be altered by any toy at any distance due to its architecture with two magnets adjusted in opposite directions. Conclusion: This is the first report describing changes in the pressure setting of some adjustable valves caused by magnetic toys in close contact. Parents, surgeons, neurologists, pediatric oncologists, and paramedics should be informed about the potential dangers of magnetic toys to prevent unwanted changes to pressure setting

Surgical resection of pediatric skull base meningiomas

Purpose: Meningiomas in children are rare, especially those located at the skull base. In this study, we report our experience of meningioma surgery in the pediatric population and compare our findings of skull base (SB) versus non-skull base (NSB) meningiomas. Methods: From our database of 724 surgically treated meningioma patients at the University Hospital, Zurich between 1995 and 2010, 12 patients under 18years of age were identified. Data for those patients was retrospectively collected through chart review. A descriptive comparison between SB and NSB meningiomas was undertaken to determine statistical significance. Results: In all 12 children (seven males, five females; mean age 12.2 ± 4.3years), surgical removal of the meningioma was performed microsurgically with a mean follow-up of 53months (range 12-137months). Of the 12 tumors, six were located in the SB and six in the NSB. Comparing SB to NSB lesions, the mean age was 11 ± 3.8 versus 14 ± 4.6years, male/female gender distribution was 5:1 compared to 1:5, mean tumor size was 7.5 ± 6.2 versus 26 ± 15.8cm2 (p = 0.03), and mean surgery time was 347 versus 214min. While WHO grade was similar for both groups, the Simpson grade revealed more extensive resection for NSB meningiomas. The Glasgow Outcome Scale at last follow-up was favorable for both groups. Conclusions: Meningioma surgery was safe with favorable outcomes. SB meningiomas were significantly smaller in size, were less likely to undergo complete resection, and had a predilection for younger, male patient

Does diagnostic delay result in decreased survival in paediatric brain tumours?

To study the hypothesis that a delay in the diagnosis of paediatric brain tumours results in decreased survival outcome probability, we compared the prediagnostic period of 315 brain tumour patients (median age 6.7years, range, 0 to 16years) with progression-free and overall survival. The median prediagnostic symptomatic interval was 60days (range, 0 to 3,480days), with a median parental delay of 14days (range, 0 to 1,835days) and a median doctor's delay of 14days (range, 0 to 3,480days). The prediagnostic symptomatic interval correlated significantly with the patient age, tumour histology, tumour location and year of diagnosis, but not with gender. We then grouped the patients according to histology (low-grade glioma [n=77], medulloblastoma [n=57], high-grade glioma [n=40], craniopharyngioma [n=27], ependymoma [n=20] and germ cell tumours [n=18]). Contrary to common belief, long prediagnostic symptomatic interval or long doctor's delay did not result in decreased survival outcome probability in any of these groups. The effect of tumour biology on survival seems to be dominant and overwhelms any possible opposing effect on survival of a delay in diagnosi

Cooperation of Striatin 3 and MAP4K4 promotes growth and tissue invasion

MAP4K4 is associated with increased motility and reduced proliferation in tumor cells, but the regulation of this dichotomous functionality remained elusive. We find that MAP4K4 interacts with striatin 3 and 4 (STRN3/4) and that STRN3 and MAP4K4 exert opposing functions in Hippo signaling and clonal growth. However, depletion of either STRN3 or MAP4K4 in medulloblastoma cells reduces invasion, and loss of both proteins abrogates tumor cell growth in the cerebellar tissue. Mechanistically, STRN3 couples MAP4K4 to the protein phosphatase 2A, which inactivates growth repressing activities of MAP4K4. In parallel, STRN3 enables growth factor-induced PKCθ activation and direct phosphorylation of VASPS157 by MAP4K4, which both are necessary for efficient cell invasion. VASPS157 directed activity of MAP4K4 and STRN3 requires the CNH domain of MAP4K4, which mediates its interaction with striatins. Thus, STRN3 is a master regulator of MAP4K4 function, and disruption of its cooperation with MAP4K4 reactivates Hippo signaling and represses tissue invasion in medulloblastoma

Author Correction: Cooperation of Striatin 3 and MAP4K4 promotes growth and tissue invasion

MAP4K4 is associated with increased motility and reduced proliferation in tumor cells, but the regulation of this dichotomous functionality remained elusive. We find that MAP4K4 interacts with striatin 3 and 4 (STRN3/4) and that STRN3 and MAP4K4 exert opposing functions in Hippo signaling and clonal growth. However, depletion of either STRN3 or MAP4K4 in medulloblastoma cells reduces invasion, and loss of both proteins abrogates tumor cell growth in the cerebellar tissue. Mechanistically, STRN3 couples MAP4K4 to the protein phosphatase 2A, which inactivates growth repressing activities of MAP4K4. In parallel, STRN3 enables growth factor-induced PKCθ activation and direct phosphorylation of VASPS157 by MAP4K4, which both are necessary for efficient cell invasion. VASPS157 directed activity of MAP4K4 and STRN3 requires the CNH domain of MAP4K4, which mediates its interaction with striatins. Thus, STRN3 is a master regulator of MAP4K4 function, and disruption of its cooperation with MAP4K4 reactivates Hippo signaling and represses tissue invasion in medulloblastoma

Incidental findings of mass lesions on neuroimages in children

Increasing use of neuroimaging in children has led to more incidental findings of CNS mass lesions, the management of which is uncertain. The authors' aims in this study are to describe these mass lesions and their evolution, as well as to discuss the management options and determine the prevalence of incidental CNS mass lesions at their pediatric clinic. A retrospective study was undertaken in children with primary CNS tumors who were younger than 18 years old and were admitted to the University Children's Hospital of Zurich, Switzerland, between January 1995 and December 2010. In 19 (5.7%) of 335 patients with newly diagnosed CNS tumors, the diagnosis of a CNS mass lesion was an incidental finding. Reasons for obtaining neuroimages in these 19 patients were head trauma (in 6 patients); research protocols (in 3); nasal/orbital malformations (in 2); endocrinological and psychiatric evaluations (in 2); and vertebral bone anomaly without neurological signs, absence seizures, congenital ataxia, recurrent vomiting, developmental delay, and "check-up" at the explicit request of the parents (in 1 patient each). Seven patients underwent immediate surgery for low-grade glioma (4 patients) and craniopharyngioma, ependymoma, and choroid plexus papilloma (1 patient each); and 12 were treated conservatively or were observed. Ten of 12 conservatively treated patients remained stable (median follow-up time 1.8 years) and the other 2 underwent delayed surgery because of tumor progression (medulloblastoma in one patient and fibrillary astrocytoma in the other). Clinicians are increasingly challenged by the discovery of incidental CNS mass lesions. A subgroup of such lesions (with typical imaging patterns such as tectal glioma and dysembryoplastic neuroepithelial tumor) can be monitored conservatively, clinically, and radiographically. Future prospective studies are needed to define optimal management strategies based on larger collections of natural histories, as well as to assess the true prevalence of incidental CNS mass lesions