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وهو من أحدث الكتب التي تناقش بصورة معمقة وموسعة فلسفة التربية والتعليم في العالم المعاصر. يتناول الكتاب تربية الطفل السعيد وتعليمه ويرتكز على افتراض أن الطفل يمتلك قدرة فطرية لتحقيق السعادة والتعلم الذي أعاقته كثرة المنظرين والنظريات إضافة إلى أنه محاولة لبحث احتمالات توفير فرص لنمو الطفل في إطار علاقاته مع والديه وأقرانه وأسرته ومجتمعه دون التدخل المعيق وغير المنطقي لما يسمى اليوم بالتعليم. ويطرح كتاب \"الطفل السعيد\" موضوع إعادة توجيه التعليم وتغيير هدفه تغييرا جذريا وهل تستطيع التربية والتعليم التحول من نموذجها الحالي الذي يسعى إلى تحويل الأطفال إلى عناصر في الإنتاج الاقتصادي أو إلى تجربة فاعلة في تحقيق الإبداع الأمثل عند الطفل بمفهومه الشامل. ويرى المؤلف أننا \"انشغلنا بتربية أبنائنا إلى الحد الذي أنسانا جوهر العملية التربوية وهو إيجاد حياة سعيدة والحياة السعيدة ليست المطلب الوحيد الذي نسعى لتوفيره لأطفالنا فحسب بل لأنفسنا أيضا. ترجم الكتاب إلى اللغة العربية الدكتور شحذة إسماعيل فالح الحاصل على الدكتوراه في اللغويات من جامعة كانساس الأميركية عام 1988 وعمل أستاذا للغويات والترجمة في الجامعة الأردنية ثم انتقل إلى جامعة الشارقة عام 2001 وما زال على رأس عمله. ونشر المترجم العديد من مقالاته في اللغويات والترجمة وترجم العديد من الكتب من الإنجليزية إلى العربية منها \"تعليم الديموقراطية\" و \"المبتكرون\" و \"التعليم العالي في مجتمع متعلم\" إضافة إلى \"لعبة الإعلام في عصر التلفاز\" و \"قراءات أساسية في الديموقراطية الأميركية.

Purpose We evaluated the American College of Medical Genetics and Genomics/Association for Molecular Pathology (ACMG/AMP) variant pathogenicity guidelines for internal consistency and compatibility with Bayesian statistical reasoning. Methods The ACMG/AMP criteria were translated into a naive Bayesian classifier, assuming four levels of evidence and exponentially scaled odds of pathogenicity. We tested this framework with a range of prior probabilities and odds of pathogenicity. Results We modeled the ACMG/AMP guidelines using biologically plausible assumptions. Most ACMG/AMP combining criteria were compatible. One ACMG/AMP likely pathogenic combination was mathematically equivalent to pathogenic and one ACMG/AMP pathogenic combination was actually likely pathogenic. We modeled combinations that include evidence for and against pathogenicity, showing that our approach scored some combinations as pathogenic or likely pathogenic that ACMG/AMP would designate as variant of uncertain significance (VUS). Conclusion By transforming the ACMG/AMP guidelines into a Bayesian framework, we provide a mathematical foundation for what was a qualitative heuristic. Only 2 of the 18 existing ACMG/AMP evidence combinations were mathematically inconsistent with the overall framework. Mixed combinations of pathogenic and benign evidence could yield a likely pathogenic, likely benign, or VUS result. This quantitative framework validates the approach adopted by the ACMG/AMP, provides opportunities to further refine evidence categories and combining rules, and supports efforts to automate components of variant pathogenicity assessments.

In 2015, professional guidelines defined the term ‘likely pathogenic’ to mean with a 90% chance of pathogenicity. To determine whether current practice reflects this definition, ClinVar classifications were tracked from 2016 to 2019. During that period, between 83.8 and 99.1% of likely pathogenic classifications were reclassified as pathogenic, depending on whether LP to VUS reclassifications are included and on how these classifications are categorized.

Our perceptual systems detect information about how our body is moving relative to the surrounding environment. Such information is essential to our ability to maintain upright standing balance. Real-time postural feedback systems are technologies that appear to enhance our ability to detect information about the movements of our body, and as a consequence improve our capacity to control the posture of our body. Here we examine a system in which real-time measurements of head position were “felt” as changes in the intensity of vibration of tactors in a headband. Using this system, participants were able to stabilize their body posture, showing a reduction in the magnitude of head sway fluctuations of more than 40% under single and dual tasking conditions. To examine this effect, we used a dynamical model that assumes that observed magnitudes of postural fluctuations reflect combined effects of underlying deterministic and stochastic dynamical processes. We derived estimates of model parameters, λ and Q . λ measures attractor strength, it quantifies the influence of the deterministic process that cause postural fluctuations to tend to drift towards a desired state. Q measures noise, it quantifies the destabilizing effects of internal perturbations and background/physiological variability in the postural control system. We find that use of our head position feedback system led to marked increases in attractor strength. This increase in attractor strength was accompanied by a marked increase in noise. When we linearly increased the resolution of feedback—by narrowing the width of the tactor activation function—we observed an approximately linear increase in attractor strength together with a non-linear increase in noise. These results suggest that use of a real-time postural feedback systems can increase the stability of postural control, but that this benefit is limited by significant accompanying exacerbations of noise being introduced into the postural control system.

We show that the human voice has complex acoustic qualities that are directly coupled to peripheral musculoskeletal tensioning of the body, such as subtle wrist movements. In this study, human vocalizers produced a steady-state vocalization while rhythmically moving the wrist or the arm at different tempos. Although listeners could only hear and not see the vocalizer, they were able to completely synchronize their own rhythmic wrist or arm movement with the movement of the vocalizer which they perceived in the voice acoustics. This study corroborates recent evidence suggesting that the human voice is constrained by bodily tensioning affecting the respiratory–vocal system. The current results show that the human voice contains a bodily imprint that is directly informative for the interpersonal perception of another’s dynamic physical states

Background The American College of Medical Genetics and Genomics (ACMG)/Association for Molecular Pathology (AMP) clinical variant interpretation guidelines established criteria for different types of evidence. This includes the strong evidence codes PS3 and BS3 for “well-established” functional assays demonstrating a variant has abnormal or normal gene/protein function, respectively. However, they did not provide detailed guidance on how functional evidence should be evaluated, and differences in the application of the PS3/BS3 codes are a contributor to variant interpretation discordance between laboratories. This recommendation seeks to provide a more structured approach to the assessment of functional assays for variant interpretation and guidance on the use of various levels of strength based on assay validation. Methods The Clinical Genome Resource (ClinGen) Sequence Variant Interpretation (SVI) Working Group used curated functional evidence from ClinGen Variant Curation Expert Panel-developed rule specifications and expert opinions to refine the PS3/BS3 criteria over multiple in-person and virtual meetings. We estimated the odds of pathogenicity for assays using various numbers of variant controls to determine the minimum controls required to reach moderate level evidence. Feedback from the ClinGen Steering Committee and outside experts were incorporated into the recommendations at multiple stages of development. Results The SVI Working Group developed recommendations for evaluators regarding the assessment of the clinical validity of functional data and a four-step provisional framework to determine the appropriate strength of evidence that can be applied in clinical variant interpretation. These steps are as follows: (1) define the disease mechanism, (2) evaluate the applicability of general classes of assays used in the field, (3) evaluate the validity of specific instances of assays, and (4) apply evidence to individual variant interpretation. We found that a minimum of 11 total pathogenic and benign variant controls are required to reach moderate-level evidence in the absence of rigorous statistical analysis. Conclusions The recommendations and approach to functional evidence evaluation described here should help clarify the clinical variant interpretation process for functional assays. Further, we hope that these recommendations will help develop productive partnerships with basic scientists who have developed functional assays that are useful for interrogating the function of a variety of genes.

Background The majority of clinical genetic testing focuses almost exclusively on regions of the genome that directly encode proteins. The important role of variants in non-coding regions in penetrant disease is, however, increasingly being demonstrated, and the use of whole genome sequencing in clinical diagnostic settings is rising across a large range of genetic disorders. Despite this, there is no existing guidance on how current guidelines designed primarily for variants in protein-coding regions should be adapted for variants identified in other genomic contexts. Methods We convened a panel of nine clinical and research scientists with wide-ranging expertise in clinical variant interpretation, with specific experience in variants within non-coding regions. This panel discussed and refined an initial draft of the guidelines which were then extensively tested and reviewed by external groups. Results We discuss considerations specifically for variants in non-coding regions of the genome. We outline how to define candidate regulatory elements, highlight examples of mechanisms through which non-coding region variants can lead to penetrant monogenic disease, and outline how existing guidelines can be adapted for the interpretation of these variants. Conclusions These recommendations aim to increase the number and range of non-coding region variants that can be clinically interpreted, which, together with a compatible phenotype, can lead to new diagnoses and catalyse the discovery of novel disease mechanisms.