A Consumer-tier based Visual-Brain Machine Interface for Augmented Reality Glasses Interactions

Objective.Visual-Brain Machine Interface(V-BMI) has provide a novel interaction technique for Augmented Reality (AR) industries. Several state-of-arts work has demonstates its high accuracy and real-time interaction capbilities. However, most of the studies employ EEGs devices that are rigid and difficult to apply in real-life AR glasseses application sceniraros. Here we develop a consumer-tier Visual-Brain Machine Inteface(V-BMI) system specialized for Augmented Reality(AR) glasses interactions. Approach. The developed system consists of a wearable hardware which takes advantages of fast set-up, reliable recording and comfortable wearable experience that specificized for AR glasses applications. Complementing this hardware, we have devised a software framework that facilitates real-time interactions within the system while accommodating a modular configuration to enhance scalability. Main results. The developed hardware is only 110g and 120x85x23 mm, which with 1 Tohm and peak to peak voltage is less than 1.5 uV, and a V-BMI based angry bird game and an Internet of Thing (IoT) AR applications are deisgned, we demonstrated such technology merits of intuitive experience and efficiency interaction. The real-time interaction accuracy is between 85 and 96 percentages in a commercial AR glasses (DTI is 2.24s and ITR 65 bits-min ). Significance. Our study indicates the developed system can provide an essential hardware-software framework for consumer based V-BMI AR glasses. Also, we derive several pivotal design factors for a consumer-grade V-BMI-based AR system: 1) Dynamic adaptation of stimulation patterns-classification methods via computer vision algorithms is necessary for AR glasses applications; and 2) Algorithmic localization to foster system stability and latency reduction.Comment: 15 pages,10 figure

Identification of <em>CHIP</em> as a novel causative gene for autosomal recessive cerebellar ataxia

Autosomal recessive cerebellar ataxias are a group of neurodegenerative disorders that are characterized by complex clinical and genetic heterogeneity. Although more than 20 disease-causing genes have been identified, many patients are still currently without a molecular diagnosis. In a two-generation autosomal recessive cerebellar ataxia family, we mapped a linkage to a minimal candidate region on chromosome 16p13.3 flanked by single-nucleotide polymorphism markers rs11248850 and rs1218762. By combining the defined linkage region with the whole-exome sequencing results, we identified a homozygous mutation (c.493CT) in CHIP (NM_005861) in this family. Using Sanger sequencing, we also identified two compound heterozygous mutations (c.389AT/c.441GT; c.621C>G/c.707GC) in CHIP gene in two additional kindreds. These mutations co-segregated exactly with the disease in these families and were not observed in 500 control subjects with matched ancestry. CHIP colocalized with NR2A, a subunit of the N-methyl-D-aspartate receptor, in the cerebellum, pons, medulla oblongata, hippocampus and cerebral cortex. Wild-type, but not disease-associated mutant CHIPs promoted the degradation of NR2A, which may underlie the pathogenesis of ataxia. In conclusion, using a combination of whole-exome sequencing and linkage analysis, we identified CHIP, encoding a U-box containing ubiquitin E3 ligase, as a novel causative gene for autosomal recessive cerebellar ataxia

Data from: Puberty status modifies the effects of gene, lifestyle factors and their interactions on adiponectin: the BCAMS Study

Supplementary information for manuscript entitled "Puberty status modifies the effects of gene, lifestyle factors and their interactions on adiponectin: the BCAMS Study

Interaction analysis of high-risk pathological features on adjuvant chemotherapy survival benefit in stage II colon cancer patients: a multi-center, retrospective study

Abstract Background We aimed to analyze the benefit of adjuvant chemotherapy in high-risk stage II colon cancer patients and the impact of high-risk factors on the prognostic effect of adjuvant chemotherapy. Methods This study is a multi-center, retrospective study, A total of 931 patients with stage II colon cancer who underwent curative surgery in 8 tertiary hospitals in China between 2016 and 2017 were enrolled in the study. Cox proportional hazard model was used to assess the risk factors of disease-free survival (DFS) and overall survival (OS) and to test the multiplicative interaction of pathological factors and adjuvant chemotherapy (ACT). The additive interaction was presented using the relative excess risk due to interaction (RERI). The Subpopulation Treatment Effect Pattern Plot (STEPP) was utilized to assess the interaction of continuous variables on the ACT effect. Results A total of 931 stage II colon cancer patients were enrolled in this study, the median age was 63 years old (interquartile range: 54–72 years) and 565 (60.7%) patients were male. Younger patients (median age, 58 years vs 65 years; P < 0.001) and patients with the following high-risk features, such as T4 tumors (30.8% vs 7.8%; P < 0.001), grade 3 lesions (36.0% vs 22.7%; P < 0.001), lymphovascular invasion (22.1% vs 6.8%; P < 0.001) and perineural invasion (19.4% vs 13.6%; P = 0.031) were more likely to receive ACT. Patients with perineural invasion showed a worse OS and marginally worse DFS (hazardous ratio [HR] 2.166, 95% confidence interval [CI] 1.282–3.660, P = 0.004; HR 1.583, 95% CI 0.985–2.545, P = 0.058, respectively). Computing the interaction on a multiplicative and additive scale revealed that there was a significant interaction between PNI and ACT in terms of DFS (HR for multiplicative interaction 0.196, p = 0.038; RERI, -1.996; 95%CI, -3.600 to -0.392) and OS (HR for multiplicative interaction 0.112, p = 0.042; RERI, -2.842; 95%CI, -4.959 to -0.725). Conclusions Perineural invasion had prognostic value, and it could also influence the effect of ACT after curative surgery. However, other high-risk features showed no implication of efficacy for ACT in our study. Trial registration This study is registered on ClinicalTrials.gov, NCT03794193 (04/01/2019)

Genomic organization of the human CHIP gene and the domain structure of the CHIP protein.

<p>The CHIP gene consists of seven exons. The CHIP protein has two key domains: the TPR domains and the one U-box domain. The five mutations identified in CHIP are indicated with arrows. Three mutations [c.493 CγT (p.L165F); c.389A>T (p.N130I); c.441G>T (p.W147C); c.707G>C (p.S236T)] are were located between the third TPR domain and the second low complexity segment. The c.621C>G (p.Y207X) mutation encodes a truncated protein without a U-box domain and the S236T mutation is located in the U-box domain.</p

The pedigrees, brain MRIs, and CHIP mutations identified.

<p>(<b>A</b>) The pedigree of family 1 with autosomal-recessive spinocerebellar ataxia. (<b>B</b>) The brain MRI of II-5 in family 1. Panel (left): axial T1-weighted image showing atrophy of the cerebellar vermis. Panel (right): midline sagittal T1-weighted image showing cerebellar atrophy, particularly evident in the superior vermis, with enlargement of the fourth ventricle. (<b>C</b>) Sanger sequencing results of codons 164–166 in exon 1 of the CHIP gene in a WT subject (left), an individual carrying the heterozygous variant (middle), and an individual carrying the homozygous c.493C>T (p.L165F) mutation (right). (<b>D</b>) The L165F missense mutation occurred at an evolutionarily conserved amino acid (in red) in the CHIP. (<b>E</b> and <b>F</b>) The pedigrees of families 2 and 3. Sanger sequencing results of the members of these two families. The red arrows indicate the mutation sites. </p

Expression of CHIP in the mouse brain and the effect of ARCA-associcated mutations on its ability to promote the degradation of NR2A.

<p>(<b>A</b>) The expression of CHIP in the cerebellum (Cb), hippocampus (Hip), cerebral cortex (Ctx), pons (PN) and medulla oblongata (MO) of mouse brain as analyzed with immunohistochemistry. (<b>B</b>) Co-localization of CHIP (red) and calcium-binding protein calbindin D-28K (green) in Purkinje cells. (<b>C</b>) Co-localization of CHIP (red) and NR2A (green) in Cb, PN and MO. (<b>D</b>) Coexpression of flag-tagged WT, but not ARCA-associated CHIP mutants (CHIP^N130I, CHIP^W147C, CHIP^L165F, CHIP^Y207X, CHIP^S236T), with HA-Fbx2 promoted the degradation of NR2A. Expression vectors for CHIP, Fbx2 and NR2A were transfected into Human Embryonic Kidney 293 cells. At 36 h after transfection, cells were treated with cycloheximide (CHX, 100 μg/ml) and chased for different time periods. NR2A was detected with western blot using the Myc antibody. Quantitative analysis was performed using NIH ImageJ analysis software. Values represent the mean ± S.D. of three independent experiments.</p