Assistive robotic device: evaluation of intelligent algorithms

Assistive robotic devices can be used to help people with upper body disabilities gaining more autonomy in their daily life. Although basic motions such as positioning and orienting an assistive robot gripper in space allow performance of many tasks, it might be time consuming and tedious to perform more complex tasks. To overcome these difficulties, improvements can be implemented at different levels, such as mechanical design, control interfaces and intelligent control algorithms. In order to guide the design of solutions, it is important to assess the impact and potential of different innovations. This paper thus presents the evaluation of three intelligent algorithms aiming to improve the performance of the JACO robotic arm (Kinova Robotics). The evaluated algorithms are 'preset position', 'fluidity filter' and 'drinking mode'. The algorithm evaluation was performed with 14 motorized wheelchair's users and showed a statistically significant improvement of the robot's performance.Comment: 4 page

An anticipative kinematic limitation avoidance algorithm for collaborative robots : Three-dimensional case

This paper presents an anticipative robot kinematic limitation avoidance algorithm for collaborative robots. The main objective is to improve the performance and the intuitivity of physical human-robot interaction. Currently, in such interactions, the human user must focus on the task as well as on the robot configuration. Indeed, the user must pay a close attention to the robot in order to avoid limitations such as joint position limitations, singularities and collisions with the environment. The proposed anticipative algorithm aims at relieving the human user from having to deal with such limitations by automatically avoiding them while considering the user's intentions. The framework developed to manage several limitations occurring simultaneously in three-dimensional space is first presented. The algorithm is then presented and detailed for each individual limitation of a spatial RRR serial robot. Finally, experiments are performed in order to assess the performance of the algorithm

Improving cable driven parallel robot accuracy through angular position sensors

Conventionally, a cable driven parallel mechanism (CDPM) pose is obtained through the forward kinematics from measurements of the cable lengths. However, this estimation method can be limiting for some applications requiring more precision. This paper proposes to use cable angle position sensors in addition to cable length measurements in order to improve the accuracy of such mechanisms. The robot pose is first obtained individually by the cable length measurements and the cable angle position measurements. A data fusion scheme combining these two types of measurements is then proposed in order to improve the CPDM accuracy. Finally, simulations and experiments are presented in order to assess the benefits of using cable angle position sensors on the CDPM

Gpr18 agonist dampens inflammation, enhances myogenesis, and restores muscle function in models of Duchenne muscular dystrophy

Introduction: Muscle wasting in Duchenne Muscular Dystrophy is caused by myofiber fragility and poor regeneration that lead to chronic inflammation and muscle replacement by fibrofatty tissue. Our recent findings demonstrated that Resolvin-D2, a bioactive lipid derived from omega-3 fatty acids, has the capacity to dampen inflammation and stimulate muscle regeneration to alleviate disease progression. This therapeutic avenue has many advantages compared to glucocorticoids, the current gold-standard treatment for Duchenne Muscular Dystrophy. However, the use of bioactive lipids as therapeutic drugs also faces many technical challenges such as their instability and poor oral bioavailability.Methods: Here, we explored the potential of PSB-KD107, a synthetic agonist of the resolvin-D2 receptor Gpr18, as a therapeutic alternative for Duchenne Muscular Dystrophy.Results and discussion: We showed that PSB-KD107 can stimulate the myogenic capacity of patient iPSC-derived myoblasts in vitro. RNAseq analysis revealed an enrichment in biological processes related to fatty acid metabolism, lipid biosynthesis, small molecule biosynthesis, and steroid-related processes in PSB-KD107-treated mdx myoblasts, as well as signaling pathways such as Peroxisome proliferator-activated receptors, AMP-activated protein kinase, mammalian target of rapamycin, and sphingolipid signaling pathways. In vivo, the treatment of dystrophic mdx mice with PSB-KD107 resulted in reduced inflammation, enhanced myogenesis, and improved muscle function. The positive impact of PSB-KD107 on muscle function is similar to the one of Resolvin-D2. Overall, our findings provide a proof-of concept that synthetic analogs of bioactive lipid receptors hold therapeutic potential for the treatment of Duchenne Muscular Dystrophy

Kinova modular robot arms for service robotics applications

This article presents Kinova's modular robotic systems, including the robots JACO2 and MICO2, actuators and grippers. Kinova designs and manufactures robotics platforms and components that are simple, sexy and safe under two business units: Assistive Robotics empowers people living with disabilities to push beyond their current boundaries and limitations while Service Robotics empowers people in industry to interact with their environment more efficiently and safely. Kinova is based in Boisbriand, Québec, Canada. Its technologies are exploited in over 25 countries and are used in many applications, including as service robotics, physical assistance, medical applications, mobile manipulation, rehabilitation, teleoperation and in research in different areas such as computer vision, artificial intelligence, grasping, planning and control interfaces. The article describes Kinova's hardware platforms, their different control modes (position, velocity and torque), control features and possible control interfaces. Integration to other systems and application examples are also presented

Clinicopathological Relationships in an Aged Case of DOORS Syndrome With a p.Arg506X Mutation in the ATP6V1B2 Gene

DOORS [deafness, onychodystrophy, osteodystrophy, intellectual disability (mental retardation), and seizures] syndrome can be caused by mutations in the TBC1D24 and ATP6V1B2 genes, both of which are involved in endolysosomal function. Because of its extreme rarity, to date, no detailed neuropathological assessment has been performed to establish clinicopathological relationships and, thereby, understand better the neurobiology of this disease in aged cases. Accordingly, the aim of the current study was to highlight the clinicopathological characteristics of a novel case with a presumable de novo mutation in the ATP6V1B2 gene from a neuropathological point of view. This Caucasian male patient, who died at the age of 72 years, presented all the typical cardinal signs of DOORS syndrome. In addition, behavioral alterations, pyramidal signs, and Parkinsonism were observed. The p.R506X pathogenic mutation identified in the ATP6V1B2 gene was responsible for the clinical phenotype. The detailed neuropathological assessment revealed a limbic-predominant tauopathy in the forms of argyrophilic grain disease, primary age-related tauopathy, and age-related tau-astrogliopathy. In summary, we present the first detailed clinicopathological report of a patient with DOORS syndrome harboring a pathogenic mutation in the ATP6V1B2 gene. The demonstrated tauopathy may be considered as a consequence of lysosomal and/or mitochondrial dysfunction, similar to that found in Niemann-Pick type C disease, which is another lysosomal disorder characterized by premature neurodegenerative disorder

Mutations impairing GSK3-mediated MAF phosphorylation cause cataract, deafness, intellectual disability, seizures, and a down syndrome-like facies

Transcription factors operate in developmental processes to mediate inductive events and cell competence, and perturbation of their function or regulation can dramatically affect morphogenesis, organogenesis, and growth. We report that a narrow spectrum of amino-acid substitutions within the transactivation domain of the v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog (MAF), a leucine zipper-containing transcription factor of the AP1 superfamily, profoundly affect development. Seven different de novo missense mutations involving conserved residues of the four GSK3 phosphorylation motifs were identified in eight unrelated individuals. The distinctive clinical phenotype, for which we propose the eponym Aymé-Gripp syndrome, is not limited to lens and eye defects as previously reported for MAF/Maf loss of function but includes sensorineural deafness, intellectual disability, seizures, brachycephaly, distinctive flat facial appearance, skeletal anomalies, mammary gland hypoplasia, and reduced growth. Disease-causing mutations were demonstrated to impair proper MAF phosphorylation, ubiquitination and proteasomal degradation, perturbed gene expression in primary skin fibroblasts, and induced neurodevelopmental defects in an in vivo model. Our findings nosologically and clinically delineate a previously poorly understood recognizable multisystem disorder, provide evidence for MAF governing a wider range of developmental programs than previously appreciated, and describe a novel instance of protein dosage effect severely perturbing developmen

Genetic burden linked to founder effects in Saguenay–Lac-Saint-Jean illustrates the importance of genetic screening test availability

The Saguenay–Lac-Saint-Jean (SLSJ) region located in the province of Quebec was settled in the 19th century by pioneers issued from successive migration waves starting in France in the 17th century and continuing within Quebec until the beginning of the 20th century. The genetic structure of the SLSJ population is considered to be the product of a triple founder effect and is characterised by a higher prevalence of some rare genetic diseases. Several studies were performed to elucidate the historical, demographic and genetic background of current SLSJ inhabitants to assess the origins of these rare disorders and their distribution in the population. Thanks to the development of new sequencing technologies, the genes and the variants responsible for the most prevalent conditions were identified. Combined with other resources such as the BALSAC population database, identifying the causal genes and the pathogenic variants allowed to assess the impacts of some of these founder mutations on the population health and to design precision medicine public health strategies based on carrier testing. Furthermore, it stimulated the establishment of many public programmes. We report here a review and an update of a subset of inherited disorders and founder mutations in the SLSJ region. Data were collected from published scientific sources. This work expands the knowledge about the current frequencies of these rare disorders, the frequencies of other rare genetic diseases in this population, the relevance of the carrier tests offered to the population, as well as the current available treatments and research about future therapeutic avenues for these inherited disorders