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In 2005, the Guatemala National Secretariat of Science and Technology (Senacyt) introduced Converciencia, a program designed to connect Guatemalan scientists residing abroad with their country of origin. Converciencia has been a flagship practice for over 15 years. This program involves three main groups of participants: (i) science and technology (S&T) policy agents, (ii) the scientific community (including parts of the Guatemala scientific diaspora, GSD), and (iii) host institutions (local co-organizers, mainly universities, and research institutes). This article presents a comprehensive and balanced overview of the Converciencia program applying an in-depth analysis of its creation, evolution, leading trends, and legacies. Using a qualitative methodology and conducting a four-level analysis (descriptive, explanatory, normative, and prescriptive) allowed for the identification of nuances of this S&T practice in the context of a scientifically lagging country such as Guatemala. The detailed data collected through documentary and desk review, gray literature, focus group discussions, and semi-structured interviews resulted in a framework to highlight the strengths, weaknesses, opportunities, and threats (SWOTs) in the planning, organization, implementation, monitoring, and perception of the results achieved by Converciencia. Findings portray the contrasting views and perceptions from a single S&T practice, depending on the participating parties' roles and responsibilities. Direct participants examined how Converciencia has achieved its objectives while questioning the effectiveness and impact that the resources allocated to the initiative have yielded over time. Evidence indicates that despite the design, coordination, and evaluation limits of Converciencia, the GSD, the scientific community in Guatemala, and the host institutions are interested in the continuity of the practice. Indeed, the main recommendation involves restructuring and turning Converciencia into a robust S&T policy. Converciencia as a policy engaging the GSD could produce greater results and impacts by involving all the key actors in co-designing activities, clearly determining roles and responsibilities, and establishing performance and impact indicators for evaluation.

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Spinocerebellar ataxia type 2 (SCA2) is a redox-sensitive neurodegenerative disease affecting the cerebellum, fibre connections in the cerebellum, the peripheral nervous system, and extracerebellar central pathways. Currently, Cuba has the highest reported global rate for this disease. The aim of this review article is to summarize and discuss the current knowledge about evidence of oxidative stress during SCA2. Recent reports have suggested that ataxin 2 and other related factors contribute to the redox imbalance in this disease. It is important to recognize and clarify the molecular mechanisms associated with the redox imbalance to consider ataxias innovative approaches to counteract oxidative stress-induced tissue damage, through alternative therapeutic or nutritional intervention in SCA2 and related diseases.

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La Ataxia espinocerebelosa tipo 2 (SCA2) es una enfermedad neurodegenerativa que alcanza las mayores tasas de incidencia y de prevalencia en Holguín, Cuba. Obtener estimados probabilísticos del riesgo dependiente de la edad, de haber heredado la mutación causante de la SCA2. Fueron revisadas las historias clínicas de 748 pacientes afectados pertenecientes a 101 familias con SCA2. El diagnóstico molecular fue realizado por PCR. La edad de inicio promedio fue de 33 años, y el 50(percent) de los pacientes fueron asintomáticos antes de los 31 años de edad. El riesgo empírico fue del 50(per cent) para individuos con 7 años de edad o menos, pero en los casos con 65 años o más, el riesgo disminuyó hasta casi un 0(percent). Existe una disminución progresiva del riesgo genético para la SCA2 a medida que avanza la edad del individuo. Los resultados son presentados como un apoyo para el asesoramiento genético de individuos en riesgo…(AU)

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Patients with spinocerebellar ataxia type 2 (SCA2), develop severe pontine nuclei, inferior olives, and Purkinje cell degeneration. This form of autosomal dominant cerebellar ataxia is accompanied by progressive ataxia and dysarthria. Although the motor dysfunction is well characterized in these patients, nothing is known about their motor learning capabilities. Here we tested 43 SCA2 patients and their matched controls in prism adaptation, a kind of visuomotor learning task. Our results show that their pattern of brain damage does not entirely disrupt motor learning. Rather, patients had impaired adaptation decrement, but surprisingly a normal aftereffect. Moreover, the mutation degree could discriminate the degree of adaptation. This pattern could reflect the net contribution of two adaptive mechanisms: strategic control and spatial realignment. Accordingly, SCA2 patients show an impaired strategic control that affects the adaptation rate, but a normal spatial realignment measured through the aftereffect. Our results suggest that the neural areas subserving spatial realignment are spared in this form of spinocerebellar ataxia.

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Patients with spinocerebellar ataxia type 2 (SCA2), develop severe pontine nuclei, inferior olives, and Purkinje cell degeneration. This form ofautosomal dominant cerebellar ataxia is accompanied by progressive ataxia and dysarthria. Although the motor dysfunction is well characterizedin these patients, nothing is known about their motor learning capabilities. Here we tested 43 SCA2 patients and their matched controls in prismadaptation, a kind of visuomotor learning task. Our results show that their pattern of brain damage does not entirely disrupt motor learning. Rather,patients had impaired adaptation decrement, but surprisingly a normal aftereffect. Moreover, the mutation degree could discriminate the degreeof adaptation. This pattern could reflect the net contribution of two adaptive mechanisms: strategic control and spatial realignment. Accordingly,SCA2 patients show an impaired strategic control that affects the adaptation rate, but a normal spatial realignment measured through the aftereffect.Our results suggest that the neural areas subserving spatial realignment are spared in this form of spinocerebellar ataxia...(AU)

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