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The aim of this observational, cross-sectional study is to evaluate potential differences in kinematics, specifically range of motion (ROM) and velocity, during planar cervical movements between patients with non-traumatic chronic neck pain and disability and asymptomatic controls, while accounting for potential influencing variables of age, sex and fear of movement. The influence of pain intensity, neck disability, age, sex or fear of motion on kinematics was analyzed through robust multivariate Bayesian regression models fitted using the brms library in R. Forty-three patients with neck pain (aged 36.70 ± 13.75 years; 10 men and 33 women) and 42 asymptomatic participants (aged 32.74 ± 13.24 years; 25 men and 17 women) completed the study protocol. The presence of neck pain/disability was associated with lower ROM and peak velocity during all planar movements when considering the influence of age, sex or fear of motion, with standardized regression coefficients that had a small effect size (ranged from 0.11 to 0.28) and estimated differences of less than 2.21° in ROM and 25.61°/s in peak velocity. Although patients with chronic mechanical neck pain showed reduced ROM and peak velocity, the small effect sizes and the low estimated differences between groups question the relevance and clinical usefulness of kinematic analysis of planar movements in samples of patients similar to those included in our study. It is probable that there are differences between the groups, but it is insufficient to rely solely on kinematic variables for patient discrimination. This limitation likely arises from the substantial variability in patient kinematics.

Abstract Numerous studies are exploring the use of cell adoptive therapies to treat hematological malignancies as well as solid tumors. However, there are numerous factors that dampen the immune response, including viruses like human immunodeficiency virus. In this study, we leverage human-derived microphysiological models to reverse-engineer the HIV-immune system interaction and evaluate the potential of memory-like natural killer cells for HIV+ head and neck cancer, one of the most common tumors in patients living with human immunodeficiency virus. Here, we evaluate multiple aspects of the memory-like natural killer cell response in human-derived bioengineered environments, including immune cell extravasation, tumor penetration, tumor killing, T cell dependence, virus suppression, and compatibility with retroviral medication. Overall, these results suggest that memory-like natural killer cells are capable of operating without T cell assistance and could simultaneously destroy head and neck cancer cells as well as reduce viral latency.

Abstract Biological tissues are highly organized structures where spatial-temporal gradients (e.g., nutrients, hypoxia, cytokines) modulate multiple physiological and pathological processes including inflammation, tissue regeneration, embryogenesis, and cancer progression. Current in vitro technologies struggle to capture the complexity of these transient microenvironmental gradients, do not provide dynamic control over the gradient profile, are complex and poorly suited for high throughput applications. Therefore, we have designed Griddent, a user-friendly platform with the capability of generating controllable and reversible gradients in a 3D microenvironment. Our platform consists of an array of 32 microfluidic chambers connected to a 384 well-array through a diffusion port at the bottom of each reservoir well. The diffusion ports are optimized to ensure gradient stability and facilitate manual micropipette loading. This platform is compatible with molecular and functional spatial biology as well as optical and fluorescence microscopy. In this work, we have used this platform to study cancer progression.

Duchenne muscular dystrophy (DMD) is a devastating degenerative disease of skeletal muscles caused by loss of dystrophin, a key protein that maintains muscle integrity, which leads to progressive muscle degeneration aggravated by chronic inflammation, muscle stem cells’ (MuSCs) reduced regenerative capacity and replacement of muscle with fibroadipose tissue. Previous research has shown that pharmacological GSK-3β inhibition favors myogenic differentiation and plays an important role in modulating inflammatory processes. Isolecanoric acid (ILA) is a natural product isolated from a fungal culture displaying GSK-3β inhibitory properties. The present study aimed to investigate the proregenerative and anti-inflammatory properties of this natural compound in the DMD context. Our results showed that ILA markedly promotes myogenic differentiation of myoblasts by increasing β-Catenin signaling and boosting the myogenic potential of mouse and human stem cells. One important finding was that the GSK-3β/β-Catenin pathway is altered in dystrophic mice muscle and ILA enhances the myofiber formation of dystrophic MuSCs. Treatment with this natural compound improves muscle regeneration of dystrophic mice by, in turn, improving functional performance. Moreover, ILA ameliorates the inflammatory response in both muscle explants and the macrophages isolated from dystrophic mice to, thus, mitigate fibrosis after muscle damage. Overall, we show that ILA modulates both inflammation and muscle regeneration to, thus, contribute to improve the dystrophic phenotype.

Breast cancer is a prevalent malignancy in the present day, particularly affecting women as one of the most common forms of cancer. A significant portion of patients initially present with localized disease, for which curative treatments are pursued. Conversely, another substantial segment is diagnosed with metastatic disease, which has a worse prognosis. Recent years have witnessed a profound transformation in the prognosis for this latter group, primarily due to the discovery of various biomarkers and the emergence of targeted therapies. These biomarkers, encompassing serological, histological, and genetic indicators, have demonstrated their value across multiple aspects of breast cancer management. They play crucial roles in initial diagnosis, aiding in the detection of relapses during follow-up, guiding the application of targeted treatments, and offering valuable insights for prognostic stratification, especially for highly aggressive tumor types. Molecular markers have now become the keystone of metastatic breast cancer diagnosis, given the diverse array of chemotherapy options and treatment modalities available. These markers signify a transformative shift in the arsenal of therapeutic options against breast cancer. Their diagnostic precision enables the categorization of tumors with elevated risks of recurrence, increased aggressiveness, and heightened mortality. Furthermore, the existence of therapies tailored to target specific molecular anomalies triggers a cascade of changes in tumor behavior. Therefore, the primary objective of this article is to offer a comprehensive review of the clinical, diagnostic, prognostic, and therapeutic utility of the principal biomarkers currently in use, as well as of their clinical impact on metastatic breast cancer. In doing so, our goal is to contribute to a more profound comprehension of this complex disease and, ultimately, to enhance patient outcomes through more precise and effective treatment strategies.

The rehabilitation of children with motor disorders is mainly focused on physical interventions. Numerous studies have demonstrated the benefits of upper function using robotic exoskeletons. However, there is still a gap between research and clinical practice, owing to the cost and complexity of these devices. This study presents a proof of concept of a 3D-printed exoskeleton for the upper limb, following a design that replicates the main characteristics of other effective exoskeletons described in the literature. 3D printing enables rapid prototyping, low cost, and easy adjustment to the patient anthropometry. The 3D-printed exoskeleton, called POWERUP, assists the user’s movement by reducing the effect of gravity, thereby allowing them to perform upper limb exercises. To validate the design, this study performed an electromyography-based assessment of the assistive performance of POWERUP, focusing on the muscular response of both the biceps and triceps during elbow flexion–extension movements in 11 healthy children. The Muscle Activity Distribution (MAD) is the proposed metric for the assessment. The results show that (1) the exoskeleton correctly assists elbow flexion, and (2) the proposed metric easily identifies the exoskeleton configuration: statistically significant differences (p-value = 2.26 ⋅ 10−7 < 0.001) and a large effect size (Cohen’s d = 3.78 > 0.8) in the mean MAD value were identified for both the biceps and triceps when comparing the transparent mode (no assistance provided) with the assistive mode (anti-gravity effect). Therefore, this metric was proposed as a method for assessing the assistive performance of exoskeletons. Further research is required to determine its usefulness for both the evaluation of selective motor control (SMC) and the impact of robot-assisted therapies.

The outermost layer of the heart, the epicardium, is an essential cell population that contributes, through epithelial-to-mesenchymal transition (EMT), to the formation of different cell types and provides paracrine signals to the developing heart. Despite its quiescent state during adulthood, the adult epicardium reactivates and recapitulates many aspects of embryonic cardiogenesis in response to cardiac injury, thereby supporting cardiac tissue remodeling. Thus, the epicardium has been considered a crucial source of cell progenitors that offers an important contribution to cardiac development and injured hearts. Although several studies have provided evidence regarding cell fate determination in the epicardium, to date, it is unclear whether epicardium-derived cells (EPDCs) come from specific, and predetermined, epicardial cell subpopulations or if they are derived from a common progenitor. In recent years, different approaches have been used to study cell heterogeneity within the epicardial layer using different experimental models. However, the data generated are still insufficient with respect to revealing the complexity of this epithelial layer. In this review, we summarize the previous works documenting the cellular composition, molecular signatures, and diversity within the developing and adult epicardium.

Background and study aims In contrast with the European Society of Gastrointestinal Endoscopy (ESGE) 2013 and the US Multi-society Task Force (USMSTF) 2020 guidelines, the ESGE 2020 guideline considers patients with three to four adenomas

The knowledge of the molecular mechanisms that regulate embryonic myogenesis from early myogenic progenitors to myoblasts, as well as the emergence of adult satellite stem cells (SCs) during development, are key concepts to understanding the genesis and regenerative abilities of the skeletal muscle. Several previous pieces of evidence have revealed that the transcription factor Pitx2 might be a player within the molecular pathways controlling somite-derived muscle progenitors’ fate and SC behavior. However, the role exerted by Pitx2 in the progression from myogenic progenitors to myoblasts including SC precursors remains unsolved. Here, we show that Pitx2 inactivation in uncommitted early myogenic precursors diminished cell proliferation and migration leading to muscle hypotrophy and a low number of SCs with decreased myogenic differentiation potential. However, the loss of Pitx2 in committed myogenic precursors gave rise to normal muscles with standard amounts of SCs exhibiting high levels of Pax7 expression. This SC population includes few MYF5+ SC-primed but increased amount of less proliferative miR-106b+cells, and display myogenic differentiation defects failing to undergo proper muscle regeneration. Overall our results demonstrate that Pitx2 is required in uncommitted myogenic progenitors but it is dispensable in committed precursors for proper myogenesis and reveal a role for this transcription factor in the generation of diverse SC subpopulations.

Summary: Background: Cirrhosis is known to have a high prevalence and mortality worldwide. However, in Europe, the epidemiology of cirrhosis is possibly undergoing demographic changes, and etiologies may have changed due to improvements in standard of care. The aim of this population-based study was to analyze the trends and the course of liver cirrhosis and its complications in recent years in Germany. Methods: We analyzed the data of all hospital admissions in Germany within diagnosis-related groups from 2005 to 2018. The diagnostic records of cirrhosis and other categories of diseases were based on ICD-10-GM codes. The primary outcome measurement was in-hospital mortality. Trends were analyzed through Poisson regression of annual number of admissions. The impact of cirrhosis on overall in-hospital mortality were assessed through the multivariate multilevel logistic regression model adjusted for age, sex, and comorbidities. Findings: Of the 248,085,936 admissions recorded between 2005 and 2018, a total of 2,302,171(0•94%) were admitted with the diagnosis of cirrhosis, mainly as a comorbidity. Compared with other chronic diseases, patients admitted with cirrhosis were younger, mainly male and had the highest in-hospital mortality rate. Diagnosis of cirrhosis was an independent risk factor of in-hospital mortality with the highest odds ratio (OR:6•2[95%CI:6.1-6•3]) among all diagnoses. The prevalence of non-alcoholic fatty liver disease has increased four times from 2005 to 2018, while alcoholic cirrhosis is 20 times than other etiologies. Bleeding was found to be decreasing over time, but ascites remained the most common complication and was increasing. Interpretation: This nationwide study demonstrates that cirrhosis represents a considerable healthcare burden, as shown by the increasing in-hospital mortality, also in combination with other chronic diseases. Alcohol-related cirrhosis and complications are on the rise. More resources and better management strategies are warranted. Funding: The funders had no influence on this study.

Muscle regeneration is an important homeostatic process of adult skeletal muscle that recapitulates many aspects of embryonic myogenesis. Satellite cells (SCs) are the main muscle stem cells responsible for skeletal muscle regeneration. SCs reside between the myofiber basal lamina and the sarcolemma of the muscle fiber in a quiescent state. However, in response to physiological stimuli or muscle trauma, activated SCs transiently re-enter the cell cycle to proliferate and subsequently exit the cell cycle to differentiate or self-renew. Recent evidence has stated that SCs display functional heterogeneity linked to regenerative capability with an undifferentiated subgroup that is more prone to self-renewal, as well as committed progenitor cells ready for myogenic differentiation. Several lineage tracing studies suggest that such SC heterogeneity could be associated with different embryonic origins. Although it has been established that SCs are derived from the central dermomyotome, how a small subpopulation of the SCs progeny maintain their stem cell identity while most progress through the myogenic program to construct myofibers is not well understood. In this review, we synthesize the works supporting the different developmental origins of SCs as the genesis of their functional heterogeneity.

Background: Individuals with obesity are known to present cognitive deficits, especially in executive functions. Executive functions play an important role in health and success throughout the whole life and have been related to food decision-making and to the ability to maintain energy balance. It is possible to improve executive functions through targeted training. This would involve brain plasticity changes that could be studied through connectivity MRI. The general hypothesis of this study is that executive functions training in children with obesity can improve food choices and produce cognitive and neuroimaging changes (structural and functional connectivity), as well as improve emotional state and quality of life.Methods: Randomized controlled double-blind trial with 12-month follow-up. Thirty children with obesity will be randomly allocated into “executive training” (Cognifit with adaptive difficulty + Cogmed) or “control task” group (Cognifit without adaptive difficulty). Both groups will attend 30–45 min of individual gamified training (Cogmed and/or Cognifit systems) by iPad, five times per week during 6 weeks. Cogmed and Cognifit software are commercially available from Pearson and Cognifit, respectively. Participants will receive an iPad with both apps installed for a 6-week use. Participants will also receive counseling diet information via presentations sent to the iPad and will wear a Fitbit Flex 2 tracker to monitor daily activity and sleep patterns. Main outcomes will be cognitive, emotional, food decision, and quality-of-life measures, as well as neuroimaging measures. Participants are evaluated at baseline (T0), after treatment (T1), and 12 months since baseline (T2).Discussion: Longitudinal study with active control group and 3 time points: baseline, immediately after treatment, and 1 year after baseline. Threefold treatment: executive function training, psychoeducation, and feedback on activity/sleep tracking. We will evaluate the transfer effects of the intervention, including emotional and functional outcomes, as well as the effects on neural plasticity by connectivity MRI.Trial registration: This project has been registered in ClinicalTrials.gov (trial registration number NCT03615274), August 3, 2018.

Cardiovascular development is initiated soon after gastrulation as bilateral precardiac mesoderm is progressively symmetrically determined at both sides of the developing embryo. The precardiac mesoderm subsequently fused at the embryonic midline constituting an embryonic linear heart tube. As development progress, the embryonic heart displays the first sign of left-right asymmetric morphology by the invariably rightward looping of the initial heart tube and prospective embryonic ventricular and atrial chambers emerged. As cardiac development progresses, the atrial and ventricular chambers enlarged and distinct left and right compartments emerge as consequence of the formation of the interatrial and interventricular septa, respectively. The last steps of cardiac morphogenesis are represented by the completion of atrial and ventricular septation, resulting in the configuration of a double circuitry with distinct systemic and pulmonary chambers, each of them with distinct inlets and outlets connections. Over the last decade, our understanding of the contribution of multiple growth factor signaling cascades such as Tgf-beta, Bmp and Wnt signaling as well as of transcriptional regulators to cardiac morphogenesis have greatly enlarged. Recently, a novel layer of complexity has emerged with the discovery of non-coding RNAs, particularly microRNAs and lncRNAs. Herein, we provide a state-of-the-art review of the contribution of non-coding RNAs during cardiac development. microRNAs and lncRNAs have been reported to functional modulate all stages of cardiac morphogenesis, spanning from lateral plate mesoderm formation to outflow tract septation, by modulating major growth factor signaling pathways as well as those transcriptional regulators involved in cardiac development.

The epicardium is the outermost cell layer in the vertebrate heart that originates during development from mesothelial precursors located in the proepicardium and septum transversum. The epicardial layer plays a key role during cardiogenesis since a subset of epicardial-derived cells (EPDCs) undergo an epithelial–mesenchymal transition (EMT); migrate into the myocardium; and differentiate into distinct cell types, such as coronary vascular smooth muscle cells, cardiac fibroblasts, endothelial cells, and presumably a subpopulation of cardiomyocytes, thus contributing to complete heart formation. Furthermore, the epicardium is a source of paracrine factors that support cardiac growth at the last stages of cardiogenesis. Although several lineage trace studies have provided some evidence about epicardial cell fate determination, the molecular mechanisms underlying epicardial cell heterogeneity remain not fully understood. Interestingly, seminal works during the last decade have pointed out that the adult epicardium is reactivated after heart damage, re-expressing some embryonic genes and contributing to cardiac remodeling. Therefore, the epicardium has been proposed as a potential target in the treatment of cardiovascular disease. In this review, we summarize the previous knowledge regarding the regulation of epicardial cell contribution during development and the control of epicardial reactivation in cardiac repair after damage.

In the field of strategic marketing, the recency, frequency and monetary (RFM) variables model has been applied for years to determine how solid a database is in terms of spending and customer activity. Retailers almost never obtain data related to their customers beyond their purchase history, and if they do, the information is often out of date. This work presents a new method, based on the fuzzy linguistic 2-tuple model and the definition of product hierarchies, which provides a linguistic interpretability giving business meaning and improving the precision of conventional models. The fuzzy linguistic 2-tuple RFM model, adapted by the product hierarchy thanks to the analytical hierarchical process (AHP), is revealed to be a useful tool for including business criteria, product catalogues and customer insights in the definition of commercial strategies. The result of our method is a complete customer segmentation that enriches the clusters obtained with the traditional fuzzy linguistic 2-tuple RFM model and offers a clear view of customers’ preferences and possible actions to define cross- and up-selling strategies. A real case study based on a worldwide leader in home decoration was developed to guide, step by step, other researchers and marketers. The model was built using the only information that retailers always have: customers’ purchase ticket details.

This study evaluates and compares the suitability for child–computer interaction (CCI, the branch within human–computer interaction focused on interactive computer systems for children) of two devices: a standard computer mouse and the ENLAZA interface, a head mouse that measures the user’s head posture using an inertial sensor. A multidirectional pointing task was used to assess the motor performance and the users’ ability to learn such a task. The evaluation was based on the interpretation of the metrics derived from Fitts’ law. Ten children aged between 6 and 8 participated in this study. Participants performed a series of pre- and post-training tests for both input devices. After the experiments, data were analyzed and statistically compared. The results show that Fitts’ law can be used to detect changes in the learning process and assess the level of psychomotor development (by comparing the performance of adults and children). In addition, meaningful differences between the fine motor control (hand) and the gross motor control (head) were found by comparing the results of the interaction using the two devices. These findings suggest that Fitts’ law metrics offer a reliable and objective way of measuring the progress of physical training or therapy.

Human brain-aging is a complex, multidimensional phenomenon. Knowledge of the numerous aspects that revolve around it is therefore essential if not only the medical issues, but also the social, psychological, and legal issues related to this phenomenon are to be managed correctly. In the coming decades, it will be necessary to find solutions to the management of the progressive aging of the population so as to increase the number of individuals that achieve successful aging. The aim of this article is to provide a current overview of the physiopathology of brain aging and of the role and perspectives of neuroimaging in this context. The progressive development of neuroimaging has opened new perspectives in clinical and basic research and it has modified the concept of brain aging. Neuroimaging will play an increasingly important role in the definition of the individual's brain aging in every phase of the physiological and pathological process. However, when the process involved in age-related brain cognitive diseases is being investigated, factors that might affect this process on a clinical and behavioral level (genetic susceptibility, risks factors, endocrine changes) cannot be ignored but must, on the contrary, be integrated into a neuroimaging evaluation to ensure a correct and global management, and they are therefore discussed in this article. Neuroimaging appears important to the correct management of age-related brain cognitive diseases not only within a medical perspective, but also legal, according to a wider approach based on development of relationship between neuroscience and law. The term neurolaw, the neologism born from the relationship between these two disciplines, is an emerging field of study, that deals with various issues in the impact of neurosciences on individual rights. Neuroimaging, enhancing the detection of physiological and pathological brain aging, could give an important contribution to the field of neurolaw in elderly where the full control of cognitive and volitional functions is necessary to maintain a whole series of rights linked to legal capacity. For this reason, in order to provide the clinician and researcher with a broad view of the brain-aging process, the role of neurolaw will be introduced into the brain-aging context.

Narratives of the Economic Crisis: National Neoliberalism in Spanish Advertising (2008-2017) Narrativas da crise econômica: o neoliberalismo nacional na publicidade espanhola (2008-2017) La publicidad, además de difundir discursos sobre productos y marcas, genera representaciones específicas de la sociedad. Teniendo en cuenta la crisis económica que atraviesa España desde 2008, esta investigación tiene como objetivo identificar cuáles son las narraciones que se han desarrollado acerca de dicha crisis en la publicidad española durante el periodo de 2008 a 2017. Mediante un cuestionario realizado a 45 profesionales del sector publicitario en España, se han identificado 31 spots que hacen referencia directa a la crisis. Estos spots han sido analizados mediante un análisis de contenido cualitativo inspirado en la semiótica narrativa. Los resultados muestran tres narrativas prototípicas dominantes que se articulan alrededor de dos ejes ideológicos: el nacionalismo y el neoliberalismo. No aparecen líneas argumentales acerca de las causas de la crisis ni de sus responsables y se traslada su solución a los ciudadanos, que deben salir de ella a través de cambios de tipo cognitivo y emocional, y ejerciendo la solidaridad con sus allegados. Aquellos elementos potencialmente críticos con el neoliberalismo son desactivados al enlazarse con los discursos de las élites políticas y económicas. Para citar este artículo / to reference this article / para citar este artigo Ruiz, F. X. y Sánchez-Sánchez, C. (2019). Narrativas de la crisis económica: el nacionalneoliberalismo en la publicidad española (2008-2017). Palabra Clave, 22(2), e2228. DOI: 10.5294/pacla.2019.22.2.8 Recibido: 05/03/2018 Aceptado: 06/11/2018

During limb formation in vertebrates with free digits, the interdigital mesoderm is eliminated by a massive degeneration process that involves apoptosis and cell senescence. The degradation process is preceded by intense DNA damage in zones located close to methylated DNA, accompanied by the activation of the DNA repair response. In this study, we show that trimethylated histone 3 (H3K4me3, H3K9me3, and H3K27me3) overlaps with zones positive for 5mC in the nuclei of interdigital cells. This pattern contrasts with the widespread distribution of acetylated histones (H3K9ac and H4ac) and the histone variant H3.3 throughout the nucleoplasm. Consistent with the intense labeling of acetylated histones, the histone deacetylase genes Hdac1, Hdac2, Hdac3, and Hdac8, and at a more reduced level, Hdac10, are expressed in the interdigits. Furthermore, local treatments with the histone deacetylase inhibitor trichostatin A, which promotes an open chromatin state, induces massive cell death and transcriptional changes reminiscent of, but preceding, the physiological process of interdigit remodeling. Together, these findings suggest that the epigenetic profile of the interdigital mesoderm contributes to the sensitivity to DNA damage that precedes apoptosis during tissue regression.

The PTPN22R620W single nucleotide polymorphism increases the risk of developing multiple autoimmune diseases including type 1 diabetes, rheumatoid arthritis and lupus. PTPN22 is highly expressed in antigen presenting cells (APCs) where the expression of the murine disease associated variant orthologue (Ptpn22R619W) is reported to dysregulate pattern recognition receptor signalling in dendritic cells (DCs) and promote T-cell proliferation. Because T-cell activation is dependent on DC antigen uptake, degradation and presentation, we analysed the efficiency of these functions in splenic and GM-CSF bone marrow derived DC from wild type (WT), Ptpn22-/- or Ptpn22R619W mutant mice. Results indicated no differential ability of DCs to uptake antigen via macropinocytosis or receptor-mediated endocytosis. Antigen degradation and presentation was also equal as was WT T-cell conjugate formation and subsequent T-cell proliferation. Despite the likely presence of multiple phosphatase-regulated pathways in the antigen uptake, processing and presentation pathways that we investigated, we observed that Ptpn22 and the R619W autoimmune associated variant were dispensable. These important findings indicate that under non-inflammatory conditions there is no requirement for Ptpn22 in DC dependent antigen uptake and T-cell activation. Our findings reveal that perturbations in antigen uptake and processing, a fundamental pathway determining adaptive immune responses, are unlikely to provide a mechanism for the risk associated with the Ptpn22 autoimmune associated polymorphism.

Neck injuries and the related pain have a high prevalence and represent an important health problem. To properly diagnose and treat them, practitioners need an accurate system for measuring Cervical Range Of Motion (CROM). This article describes the development and validation of an inexpensive, small (4 cm × 4 cm × 8 cm), light (< 200 g) and easy to use solution for measuring CROM using wearable inertial sensors. The proposed solution has been designed with the clinical practice in mind, after consulting with practitioners. It is composed of: (a) two wearable wireless MEMS-based inertial devices, (b) a recording and report generation software application and (c) a measurement protocol for assessing CROM. The solution provides accurate (none of our results is outside the ROM ranges when compared with previously published results based on an optical tracking device) and reliable measurements (ICC = 0.93 for interrater reliability when compared with an optical tracking device and ICC > 0.90 for test-retest reliability), surpassing the popular CROM instrument’s capabilities and precision. It also fulfills the needs for clinical practice attending to effectiveness, efficiency (4 min from setup to final report) and user’s satisfaction (as reported by practitioners). The solution has been certified for mass-production and use in medical environments.

White matter (WM) abnormalities have already been shown in presymptomatic (Pre-HD) and symptomatic HD subjects using Magnetic Resonance Imaging (MRI). In the present study, we examined the microstructure of the long-range large deep WM tracts by applying two different MRI approaches: Diffusion Tensor Imaging (DTI) -based tractography, and T2*weighted (iron sensitive) imaging. We collected Pre-HD subjects (n = 25), HD patients (n = 25) and healthy control subjects (n = 50). Results revealed increased axial (AD) and radial diffusivity (RD) and iron levels in Pre-HD subjects compared to controls. Fractional anisotropy decreased between the Pre-HD and HD phase and AD/RD increased and although impairment was pervasive in HD, degeneration occurred in a pattern in Pre-HD. Furthermore, iron levels dropped for HD patients. As increased iron levels are associated with remyelination, the data suggests that Pre-HD subjects attempt to repair damaged deep WM years before symptoms occur but this process fails with disease progression.

En este trabajo se describe una nueva especie de thrips de suelo para Adraneothrips Hood, 1925 de Costa Rica. Se provee una clave de identificación para las especies de América Central.A new species of Adraneothrips Hood, 1925, soil Thysanoptera, is described from Costa Rica. A key for the recognition of the species of Central America is provided.

White matter abnormalities have been shown in presymptomatic and symptomatic Huntington's disease (HD) subjects using Magnetic Resonance Imaging (MRI) and Diffusion Tensor Imaging (DTI) methods. The largest white matter tract, the corpus callosum (CC), has been shown to be particularly vulnerable; however, little work has been done to investigate the regional specificity of tract abnormalities in the CC. Thus, this study examined the major callosal tracts by applying DTI-based tractography. Using TrackVis, a previously defined region of interest tractography method parcellating CC into seven major tracts based on target region was applied to 30 direction DTI data collected from 100 subjects: presymptomatic HD (Pre-HD) subjects (n=25), HD patients (n=25) and healthy control subjects (n=50). Tractography results showed decreased fractional anisotropy (FA) and increased radial diffusivity (RD) across broad regions of the CC in Pre-HD subjects. Similar though more severe deficits were seen in HD patients. In Pre-HD and HD, callosal FA and RD were correlated with Disease Burden/CAG repeat length as well as motor (UHDRSI) and cognitive (URDRS2) assessments. These results add evidence that CC pathways are compromised prior to disease onset with possible demyelination occurring early in the disease and suggest that CAG repeat length is a contributing factor to connectivity deficits. Furthermore, disruption of these callosal pathways potentially contributes to the disturbances of motor and cognitive processing that characterize HD.