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Numerous studies have been conducted to investigate the potential effect of educational robots, but what appears to be missing is an up-to-date and thorough review of the learning effectiveness of educational robots and the various influencing factors. In this study, a meta-analysis was conducted to systematically synthesize studies' findings on the effects of educational robots on students' learning outcomes. After searching for randomized studies describing educational robots interventions to improve learning outcomes, 34 effect sizes described in 17 articles met the selection criteria. The results of our work evidence a moderate but significantly positive effect of educational robots on learning outcomes (g  =  0.57, 95% CI [0.49, 0.65], p  <  0.00001). Moreover, moderator analyses were conducted to investigate important factors relating to the variation of the impact, including educational level and assessment type. Based on the findings of this study, we provide researchers and practitioners with insights into what characteristics of educational robot interventions appear to benefit students' learning outcomes and how pedagogical approaches can be applied in various educational settings to guide the design of future educational robot interventions. [ABSTRACT FROM AUTHOR]

Defective neurogenesis in the postnatal brain can lead to many neurological and psychiatric disorders, yet the mechanism behind postnatal neurogenesis remains to be investigated. Huntingtin-associated protein 1 (HAP1) participates in intracellular trafficking in neurons, and its absence leads to postnatal death in mice. Here, we used tamoxifen-induced (TM-induced) Cre recombination to deplete HAP1 in mice at different ages. We found that HAP1 reduction selectively affects survival and growth of postnatal mice, but not adults. Neurogenesis, but not gliogenesis, was affected in HAP1-null neurospheres and mouse brain. In the absence of HAP1, postnatal hypothalamic neurons exhibited reduced receptor tropomyosin-related kinase B (TRKB) levels and decreased survival. HAP1 stabilized the association of TRKB with the intracellular sorting protein sortilin, prevented TRKB degradation, and promoted its anterograde transport. Our findings indicate that intracellular sorting of neurotrophin receptors is critical for postnatal neurogenesis and could provide a therapeutic target for defective postnatal neurogenesis., Introduction Neurogenesis is the process by which neurons are generated from neural stem and progenitor cells. Unlike embryonic neurogenesis, which is largely controlled by transcription factors, and adult neurogenesis, which [...]

This paper proposes a systematic methodology for dimension synthesis, kinematics, and statics of a novel 2SPS + SPR + SP parallel manipulator with 3DOF. First, a workspace is varied and analyzed by varying the orientation of a revolute joint, and an optimum orientation of revolute joint is determined. Second, the inverse displacement is analyzed, and the formulas are derived for solving general inverse/forward velocities and accelerations. Third, the geometric constraints of constrained forces are determined and the formulas are derived for solving the active/constrained forces. [DOI: 10.1115/1.2936897] Keywords: parallel manipulator, workspace, kinematics, statics

Joubert syndrome is an autosomal recessive disorder characterized by congenital malformation of the cerebellum and brainstem, with abnormal decussation in the brain. Mutations in the Abelson helper integration site 1 gene, which encodes the protein AHI1, have been shown to cause Joubert syndrome. In this study, we found that mouse Ahi1 formed a stable complex with huntingtin-associated protein 1 (Hap1), which is critical for neonatal development and involved in intracellular trafficking. Hap1-knockout mice showed significantly reduced Ahi1 levels, defective cerebellar development, and abnormal axonal decussation. Suppression of Ahi1 also decreased the level of Hap1; and truncated Ahi1, which corresponds to the mutations in Joubert syndrome, inhibited neurite outgrowth in neuronal culture. Reducing Hap1 expression suppressed the level and internalization of TrkB, a neurotrophic factor receptor that mediates neurogenesis and neuronal differentiation, which led to decreased TrkB signaling. These findings provide insight into the pathogenesis of Joubert syndrome and demonstrate the critical role of the Ahi1-Hap1 complex in early brain development., Introduction Clinical features of Joubert syndrome (JS) include neonatal hypotonia (loss of muscle tone), ataxia, developmental delay, mental retardation, and frequently abnormalities in breathing and eye movements (1-3). Various abnormalities [...]

Non-human primates are valuable for modelling human disorders and for developing therapeutic strategies; however, little work has been reported in establishing transgenic non-human primate models of human diseases. Huntington's disease [...]

The hypothalamus responds to circulating leptin and insulin in the control of food intake and body weight. A number of neurotransmitters in the hypothalamus, including [gamma]-aminobutyric acid (GABA), also have key roles in feeding. Huntingtin-associated protein 1 (Hap1) is expressed more abundantly in the hypothalamus than in other brain regions, and lack of Hap1 in mice leads to early postnatal death. Hap1 is also involved in intracellular trafficking of the GABA[sub.A] receptor. Here, we report that fasting upregulates the expression of Hap1 in the rodent hypothalamus, whereas intracerebroventricular administration of insulin downregulates Hap1 by increasing its degradation through ubiquitination. Decreasing the expression of mouse hypothalamic Hap1 by siRNA reduces the level and activity of hypothalamic GABA[sub.A] receptors and causes a decrease in food intake and body weight. These findings provide evidence linking hypothalamic Hap1 to GABA in the stimulation of feeding and suggest that this mechanism is involved in the feeding-inhibitory actions of insulin in the brain., Author(s): Guoqing Sheng [1]; Guo-qing Chang [2]; John Y Lin [3]; Zhao-Xue Yu [1]; Zhi-Hui Fang [1]; Juan Rong [1]; Stuart A Lipton [3, 4]; Shi-Hua Li [1]; Gang Tong [...]

Author(s): Lucia Pastorino [1, 7]; Anyang Sun [1, 6, 7]; Pei-Jung Lu [2, 7]; Xiao Zhen Zhou [1]; Martin Balastik [1]; Greg Finn [1]; Gerburg Wulf [1]; Jormay Lim [1]; [...]

Huntington's disease is caused by a polyglutamine expansion in the protein huntingtin. Several studies suggest that huntingtin and its associated protein HAP1 participate in intracellular trafficking and that polyglutamine expansion affects vesicular transport. A study now provides new evidence that HAP1 is also involved in the endocytosis of membrane receptors. These studies offer insight into the normal function of HAP1 and its involvement in Huntington's disease.

Abstract A critical issue in understanding Huntington's disease (HD) pathogenesis is how the ubiquitously expressed mutant huntingtin (mhtt) with an expanded polyglutamine repeat can cause selective toxicity of striatal and cortical neurons. Two potential cellular models may contribute to such specificity: expression of mhtt in these vulnerable neurons alone may be sufficient to result in their dysfunction and/or degeneration (cell-autonomous model); or mhtt in other cell types can elicit pathological cell-cell interactions to cause the vulnerable neurons to become dysfunctional and be at risk for degeneration (cell-cell interaction model). To distinguish between these two models, we have selectively expressed a neuropathogenic fragment of mhtt-exon1 in striatal medium spiny neurons (MSNs) by crossing a conditional mouse model of HD with a striatal-specific Cre mouse line. In this striatal model of HD, we observed progressive and cell-autonomous nuclear accumulation of mhtt aggregates in MSNs. Surprisingly, unlike the mouse model expressing mhtt-exon1 in all the neurons in the brain, the striatal model lacks significant locomotor deficits and striatal neuropathology including gliosis and dark degenerating neurons. Electrophysiological findings from acutely dissociated MSNs revealed a cell-autonomous deficit in N-methyl-d-aspartate (NMDA) receptor sensitivity to Mg2+, a deficit also present in other mouse models of HD. In conclusion, this study provides the first in vivo genetic evidence that pathological cell-cell interactions are necessary for striatal pathogenesis in a conditional mouse model of HD, and suggests a ''two-hit'' hypothesis in which both cell-autonomous toxicity and pathological cell-cell interactions are critical to HD pathogenesis.

Coastal ecosystems are vulnerable to plant invasion and expected sea level rise in China. This study explored the responses of microbial communities and extracellular enzyme activity in the marsh soils of native Phragmites australis and exotic Spartina alterniflora to waterlogging and increasing salinity (to mimic prolonged inundation and saltwater intrusion) based on the determination of phospholipid fatty acids and analysis of enzyme kinetics. The results showed that waterlogging and increased salinity treatments decreased the soil microbial biomass in both P. australis and S. alterniflora soils, with waterlogging exacerbating the negative effects of salinity. Fungi/bacteria ratios decreased under both waterlogging and salinity treatments, whereas actinomycetes/bacteria ratios increased with increasing salinity. The degree of the adverse effects of salinity on plant growth of S. alterniflora and soil microbial biomass was lower than that on P. australis. Generally, waterlogging treatment increased the activity of sucrase, cellulase, urease, and dehydrogenase in S. alterniflora soil. Increased salinity decreased all the assayed extracellular enzyme activity in both P. australis and S. alterniflora soils. The synergistic effects of waterlogging and increased salinity treatments on the enzyme activities in P. australis soil were significant, whereas only the effect on the cellulase activity was significant in S. alterniflora soil. This study indicated a greater ability of the microbial community and extracellular enzyme activity of S. alterniflora soil to adapt to waterlogging and increased salinity compared with those of P. australis soil due to the lower sensitivity of S. alterniflora growth and soil nutrients to stress. [ABSTRACT FROM AUTHOR]

The development of stimuli-responsive theranostic platforms is of great demand for efficient cancer treatment because they can enhance diagnostic specificity and sensitivity. In this work, we report a pH-responsive theranostic nanoplatform based on FeOOH clusters loaded mesoporous silica nanoparticles (Fe@MSNs). The as-synthesized Fe@MSNs possess activatable T1 magnetic resonance imaging (MRI) performance that can respond to the acidic microenvironment of solid tumor to turn on T1 singals by releasing paramagnetic Fe3+ ions. The Fe@MSNs are biocompatible without appreciable cytotoxicity. Moreover, the unique mesoporous structure endows the Fe@MSNs with significant advantages to effectively deliver chemotherapeutic drug for inhibiting the growth of solid tumor. We believe that this novel pH-responsive theranostic nanoplatform holds great promise in cancer treatment. [ABSTRACT FROM AUTHOR]

Dengue virus (DENV) is one of the most widespread arboviruses. The four DENV serotypes infect about 400 million people every year, causing 96 million clinical dengue cases, of which approximately 500’000 are severe and potentially life-threatening. The only licensed vaccine has a limited efficacy and is only recommended in regions with high endemicity. We previously reported that 2’-O-methyltransferase mutations in DENV-1 and DENV-2 block their capacity to inhibit type I IFNs and render the viruses attenuated in vivo, making them amenable as vaccine strains; here we apply this strategy to all four DENV serotypes to generate a tetravalent, non-chimeric live-attenuated dengue vaccine. 2’-O-methyltransferase mutants of all four serotypes are highly sensitive to type I IFN inhibition in human cells. The tetravalent formulation is attenuated and immunogenic in mice and cynomolgus macaques and elicits a response that protects from virus challenge. These results show the potential of 2’-O-methyltransferase mutant viruses as a safe, tetravalent, non-chimeric dengue vaccine. [ABSTRACT FROM AUTHOR]