Quercetin prevents osteoarthritis progression possibly via regulation of local and systemic inflammatory cascades.

Due to the lack of effective treatments, osteoarthritis (OA) remains a challenge for clinicians. Quercetin, a bioflavonoid, has shown potent anti-inflammatory effects. However, its effect on preventing OA progression and the underlying mechanisms are still unclear. In this study, Sprague-Dawley male rats were divided into five groups: control group, OA group (monosodium iodoacetate intra-articular injection), and three quercetin-treated groups. Quercetin-treated groups were treated with intragastric quercetin once a day for 28 days. Gross observation and histopathological analysis showed cartilage degradation and matrix loss in the OA group. High-dose quercetin-group joints showed failure in OA progression. High-dose quercetin inhibited the OA-induced expression of MMP-3, MMP-13, ADAMTS4, and ADAMTS5 and promoted the OA-reduced expression of aggrecan and collagen II. Levels of most inflammatory cytokines and growth factors tested in synovial fluid and serum were upregulated in the OA group and these increases were reversed by high-dose quercetin. Similarly, subchondral trabecular bone was degraded in the OA group and this effect was reversed in the high-dose quercetin group. Our findings indicate that quercetin has a protective effect against OA development and progression possibly via maintaining the inflammatory cascade homeostasis. Therefore, quercetin could be a potential therapeutic agent to prevent OA progression in risk groups.

Notoginsenoside R1 Promotes Migration, Adhesin, Spreading, and Osteogenic Differentiation of Human Adipose Tissue-Derived Mesenchymal Stromal Cells.

Cellular activities, such as attachment, spreading, proliferation, migration, and differentiation are indispensable for the success of bone tissue engineering. Mesenchymal stromal cells (MSCs) are the key precursor cells to regenerate bone. Bioactive compounds from natural products had shown bone regenerative potential. Notoginsenoside R1 (NGR1) is a primary bioactive natural compound that regulates various biological activities, including cardiovascular protection, neuro-protection, and anti-cancer effects. However, the effect of NGR1 on migration, adhesion, spreading, and osteogenic differentiation of MSCs required for bone tissue engineering application has not been tested properly. In this study, we aimed to analyze the effect of NGR1 on the cellular activities of MSCs. Since human adipose-derived stromal cells (hASCs) are commonly used MSCs for bone tissue engineering, we used hASCs as a model of MSCs. The optimal concentration of 0.05 µg/mL NGR1 was biocompatible and promoted migration and osteogenic differentiation of hASCs. Pro-angiogenic factor VEGF expression was upregulated in NGR1-treated hASCs. NGR1 enhanced the adhesion and spreading of hASCs on the bio-inert glass surface. NGR1 robustly promoted hASCs adhesion and survival in 3D-printed TCP scaffold both in vitro and in vivo. NGR1 mitigated LPS-induced expression of inflammatory markers IL-1ß, IL-6, and TNF-α in hASCs as well as inhibited the RANKL/OPG expression ratio. In conclusion, the biocompatible NGR1 promoted the migration, adhesion, spreading, osteogenic differentiation, and anti-inflammatory properties of hASCs.

Osteocyte-Mediated Translation of Mechanical Stimuli to Cellular Signaling and Its Role in Bone and Non-bone-Related Clinical Complications.

PURPOSE OF REVIEW: Osteocytes comprise > 95% of the cellular component in bone tissue and produce a wide range of cytokines and cellular signaling molecules in response to mechanical stimuli. In this review, we aimed to summarize the molecular mechanisms involved in the osteocyte-mediated translation of mechanical stimuli to cellular signaling, and discuss their role in skeletal (bone) diseases and extra-skeletal (non-bone) clinical complications. RECENT FINDINGS: Two decades before, osteocytes were assumed as a dormant cells buried in bone matrix. In recent years, emerging evidences have shown that osteocytes are pivotal not only for bone homeostasis but also for vital organ functions such as muscle, kidney, and heart. Osteocyte mechanotransduction regulates osteoblast and osteoclast function and maintains bone homeostasis. Mechanical stimuli modulate the release of osteocyte-derived cytokines, signaling molecules, and extracellular cellular vesicles that regulate not only the surrounding bone cell function and bone homeostasis but also the distant organ function in a paracrine and endocrine fashion. Mechanical loading and unloading modulate the osteocytic release of NO, PGE2, and ATPs that regulates multiple cellular signaling such as Wnt/ß-catenin, RANKL/OPG, BMPs, PTH, IGF1, VEGF, sclerostin, and others. Therefore, the in-depth study of the molecular mechanism of osteocyte mechanotransduction could unravel therapeutic targets for various bone and non-bone-related clinical complications such as osteoporosis, sarcopenia, and cancer metastasis to bone.

A dual purpose universal influenza vaccine candidate confers protective immunity against anthrax.

Preventive influenza vaccines must be reformulated annually because of antigen shift and drift of circulating influenza viral strains. However, seasonal vaccines do not always match the circulating strains, and there is the ever-present threat that avian influenza viruses may adapt to humans. Hence, a universal influenza vaccine is needed to provide protective immunity against a broad range of influenza viruses. We designed an influenza antigen consisting of three tandem M2e repeats plus HA2, in combination with a detoxified anthrax oedema toxin delivery system (EFn plus PA) to enhance immune responses. The EFn-3×M2e-HA2 plus PA vaccine formulation elicited robust, antigen-specific, IgG responses; and was protective against heterologous influenza viral challenge when intranasally delivered to mice three times. Moreover, use of the detoxified anthrax toxin system as an adjuvant had the additional benefit of generating protective immunity against anthrax. Hence, this novel vaccine strategy could potentially address two major emerging public health and biodefence threats.

Fish gelatin films incorporated with cinnamaldehyde and its sulfobutyl ether-ß-cyclodextrin inclusion complex and their application in fish preservation.

For food preservation, the packaging film needs to have higher antibacterial activity in initial phase and keep longer activity. In this study, cinnamaldehyde (CA) and its sulfobutyl ether-ß-cyclodextrin inclusion complex (CA/S) were used to fabricate fish gelatin antibacterial composite films. The addition enhanced the elongation at break and light barrier property of the films. Film forming solution incorporated with CA and CA/S presented the most excellent inhibition ratio against Pseudomonas aeruginosa, which was 98.43 ± 1.11% in initial period and still 82.97 ± 4.55% at 72 h. Further, the packaging solution of gelatin combined CA and CA/S effectively inhibited the growth of microorganisms during preservation of grass carp slices. Especially, the total volatile salt-based nitrogen (TVB-N) did not exceed 10 mg/100 g at the end of storage, indicating that the active coating could obviously extend the shelf life of fish muscle. This work provided a promising food packaging system with antimicrobial and environmentally friendly.

Coating 3D-Printed Bioceramics with Histatin Promotes Adhesion and Osteogenesis of Stem Cells.

Mesenchymal stem cell and 3D printing-based bone tissue engineering present a promising technique to repair large-volume bone defects. Its success is highly dependent on cell attachment, spreading, osteogenic differentiation, and in vivo survival of stem cells on 3D-printed scaffolds. In this study, we applied human salivary histatin-1 (Hst1) to enhance the interactions of human adipose-derived stem cells (hASCs) on 3D-printed ß-tricalcium phosphate (ß-TCP) bioceramic scaffolds. Fluorescent images showed that Hst1 significantly enhanced the adhesion of hASCs to both bioinert glass and 3D-printed ß-TCP scaffold. In addition, Hst1 was associated with significantly higher proliferation and osteogenic differentiation of hASCs on 3D-printed ß-TCP scaffolds. Moreover, coating 3D-printed ß-TCP scaffolds with histatin significantly promotes the survival of hASCs in vivo. The ERK and p38 but not JNK signaling was found to be involved in the superior adhesion of hASCs to ß-TCP scaffolds with the aid of Hst1. In conclusion, Hst1 could significantly promote the adhesion, spreading, osteogenic differentiation, and in vivo survival of hASCs on 3D-printed ß-TCP scaffolds, bearing a promising application in stem cell/3D printing-based constructs for bone tissue engineering.

A new self-attenuated therapeutic influenza vaccine that uses host cell-restricted attenuation by artificial microRNAs.

New strategies are urgently needed for developing vaccines and/or anti-viral drugs against influenza viruses, because antigenic shift and drift inevitably occurs in circulating strains each year, and new strains resistant to anti-viral drugs have recently emerged. In our study, we designed and incorporated artificial microRNAs (amiRNAs) into the NA segment of rescued influenza viruses to separately target two host genes, Cdc2-like kinase 1 (CLK1) and SON DNA binding protein (SON), which were found to play an essential role in virus replication. Mouse epithelial fibroblast (MEF) or human lung carcinoma A549 cells infected with engineered influenza PR8 viruses expressing amiR-30CLK1 (PR8-amiR-30CLK1) or amiR-93SON (PR8-amiR-93SON) had reduced expression of host proteins CLK1 and SON, respectively. All engineered influenza viruses functioned as attenuated vaccines, induced significantly higher antibody responses, and provided greater protective efficacy. In addition, they were found to be safe, based on the mouse weight changes and clinical signs observed. In contrast to the engineered viruses targeting SON, mice treated with engineered viruses targeting CLK1 recovered from weight loss and survived lethal infection by 6 h after lethal-dose PR8 infection, suggesting that our PR8-amiR-30CLK1 self-attenuated influenza virus (SAIV) could be used as a new therapeutic influenza vaccine.

The role of oral microbiome in respiratory health and diseases.

The oral cavity (mouth) has various microbial habitats, including, teeth, gingival sulcus, gingiva, tongue, inner cheek, hard palate, and soft palate. The human oral cavity houses the second most diverse microbiome in the body harboring over 700 bacterial species. The fine-tuned equilibrium of the oral microbiome ecosystem maintains oral health. Oral dysbiosis caused by food habits and poor oral hygiene leads to various oral diseases such as periodontitis, caries, gingivitis, and oral cancer. Recent advances in technology have revealed the correlation between the oral microbiome and systemic diseases such as pulmonary diseases, cardiovascular diseases, rheumatoid arthritis, Alzheimer's disease, and other metabolic diseases. Since the oral cavity directly connects with the upper respiratory tract, the oral microbiome has easier access to the respiratory system compared to other organ systems. Direct aspiration of oral microflora in the respiratory system and oral dysbiosis-induced host immune reaction and inflammation are mainly responsible for various pulmonary complications. Numbers of literature have reported the correlation between oral diseases and pulmonary diseases, suggesting the possible role of the oral microbiome in respiratory diseases such as chronic obstructive pulmonary diseases, pneumonia, lung cancer, etc. This paper reviews the current evidence in establishing a link between the oral microbiome and pulmonary diseases. We also discuss future research directions focusing on the oral microbiome to unravel novel therapeutic approaches that could prevent or treat the various pulmonary complications.

Lactobacillus acidipiscis Induced Regulatory Gamma Delta T Cells and Attenuated Experimental Autoimmune Encephalomyelitis.

Multiple sclerosis is a chronic autoimmune disease involving the central nervous system, and shows a high disability rate. Its pathogenesis is complicated, and there is no good treatment. In recent years, with in-depth studies on the regulation of gastrointestinal flora, the relationship between the mammalian immune system and the intestinal flora has been extensively explored. Changes in the composition and structure of the gastrointestinal flora can affect the characteristics and development of the host immune system and even induce a series of central nervous system inflammation events. The occurrence and development of multiple sclerosis are closely related to the continuous destruction of the intestinal barrier caused by intestinal dysbacteriosis. In this study, we analyzed Lactobacillus acidipiscis in a mouse model of experimental autoimmune encephalomyelitis (EAE). We found that the amount of L. acidipiscis in the intestinal tract was inversely proportional to the progress of EAE development. In addition, the number of CD4+ FOXP3+ regulatory T cells in the mesenteric lymph nodes of mice increased significantly after the mice were fed with L. acidipiscis, and the differentiation of CD4+ T cells to Th1 and Th17 cells was inhibited. However, the protective effect of L. acidipiscis was lost in γδ T cell-deficient mice and hence was concluded to depend on the presence of regulatory γδ T cells in the intestinal epithelium. Moreover, including L. acidipiscis enhanced the development of Vγ1+γδ T cells but suppressed that of Vγ4+γδ T cells. In summary, our results demonstrated the ability of L. acidipiscis to induce generation of regulatory γδ T cells that suppress the development of the encephalomyelitic Th1 and Th17 cells and the progress of EAE.

Downregulation of Macrophage-Specific Act-1 Intensifies Periodontitis and Alveolar Bone Loss Possibly via TNF/NF-κB Signaling.

Periodontitis is a chronic inflammatory oral disease that affects almost half of the adult population. NF-κB activator 1 (Act1) is mainly expressed in immune cells, including macrophages, and modulates immune cells' function to regulate inflammation in inflammatory diseases. Macrophages play a vital role in the pathophysiology of periodontitis. However, the effect of macrophage-specific Act1 on periodontitis has not been investigated yet. This study aims to unravel the role of macrophage-specific Act1 on the pathophysiology of periodontitis. The expression of Act1 in healthy and periodontitis periodontal tissue was confirmed by immunohistochemistry. Macrophage-specific Act1 expression downregulated (anti-Act1) mice were developed by inserting anti-Act1 antisense oligonucleotides after the CD68 promoter of C57BL/6 mice. Ligature-induced periodontitis (LIP) was induced in anti-Act1 mice and wildtype mice. Micro-CT, histology, and TRAP staining analyzed the periodontal tissue status, alveolar bone loss, and osteoclast numbers. Immunohistochemistry, RT-qPCR, and ELISA analyzed the inflammatory cells infiltration, expression of inflammatory cytokines, and M1/M2 macrophage polarization. mRNA sequencing of in vitro bacterial lipopolysaccharide (LPS)-treated peritoneal macrophages analyzed the differentially expressed genes in anti-Act1 mice during inflammation. Anti-Act1 mice showed aggravated periodontitis and alveolar bone loss compared to wildtype. Periodontitis-affected periodontal tissue (PAPT) of anti-Act1 mice showed a higher degree of macrophage infiltration, and M1 macrophage polarization compared to wildtype. Levels of pro-inflammatory cytokines (IL-1ß, IL-6, and TNFα), and macrophage activity-related factors (CCL2, CCL3, and CCL4) were robustly high in PAPT of anti-Act1 mice compared to wildtype. mRNA sequencing and KEGG analysis showed activated TNF/NF-κB signaling in LPS-treated macrophages from anti-Act1 mice. In vitro studies on LPS-treated peritoneal macrophages from anti-act1 mice showed a higher degree of cell migration and expression of inflammatory cytokines, macrophage activity-related factors, M1 macrophage-related factors, and TNF/NF-κB signaling related P-p65 protein. In conclusion, downregulation of macrophage-specific Act1 aggravated periodontitis, alveolar bone loss, macrophage infiltration, inflammation, and M1 macrophage polarization. Furthermore, LPS-treated macrophages from anti-Act1 mice activated TNF/NF-κB signaling. These results indicate the distinct role of macrophage-specific Act1 on the pathophysiology of periodontitis possibly via TNF/NF-κB signaling.

miR-146a Overexpression in Oral Squamous Cell Carcinoma Potentiates Cancer Cell Migration and Invasion Possibly via Targeting HTT.

Huntingtin (HTT) is one of the target genes of miR-146-a and regulates various cancer cell activities. This study aims to explore the miR-146a expression pattern in oral squamous cell carcinoma (OSCC) and its role and mechanism in OSCC progression and metastasis via targeting the HTT gene. OSCC tissue and non-cancerous matched tissue (NCMT) were obtained from 14 patients. OSCC cell lines and normal HOK cells were used to analyze migration and invasion assay. OSCC-induced miR-146a knockout mice (B6.Cg-Mir146tm1.1Bal) model was developed. Transwell cell migration/invasion and scratch wound assays were used to investigate the OSCC cell migration and invasion in vitro. Kaplan-Meier survival analysis was used to investigate the association of HTT expression patterns in cancer tissue with patient survival percentage and duration. Pearson's correlation analysis tested the association between miR-146a and HTT expression in OSCC tissues. miR-146a mimic and inhibitor transfection were performed to overexpress and knockdown the miR-146a in OSCC cells, respectively. miR-146a expression was highly upregulated in OSCC tissues and OSCC cell lines. Cancer cell migration/invasion was enhanced in miR-146a overexpressed cells and reduced in mi-R146a knockdowned cells. HTT expression was reduced in OSCC tissues and cell lines compared to NCMT and HOK cells, respectively. HTT expression was downregulated in miR-146a overexpressed OSCC cells and upregulated in miR-146a knockdowned OSCC cells. The expression pattern of miR-146a in OSCC cell lines and tissues was inversely correlated with HTT expression. Prediction of miRNA target analysis showed that HTT possesses the binding sites for miR-146a. HTT overexpression in OSCC tissues was associated with patients' higher survival percentage and duration. HTT knockdown in OSCC cells enhanced miR-146a expression and cell migration/invasion. Inducing OSCC in miR-146a knockout mice increased the HTT expression in tongue tissue and alleviated the cancer aggressiveness and epithelial damage. Overexpressed miR-146a in OSCC targets the HTT gene and enhances cancer cell migration/invasion unraveling the possible role of HTT in miR146a-mediated OSCC cell migration and invasion.

SLIT2 Overexpression in Periodontitis Intensifies Inflammation and Alveolar Bone Loss, Possibly via the Activation of MAPK Pathway.

SLIT2, a member of neuronal guidance cues, has been reported to regulate inflammation and cancer progression. Periodontitis is an oral inflammatory disease that degenerates periodontal tissue, alveolar bone and tooth. This study aims to explore the expression pattern of SLIT2 in periodontitis and its role in disease progression and bone loss. Gingival tissue of 20 periodontitis patients and 20 healthy-controls was obtained. Ligature-induced periodontitis (LIP) mice-model was developed in Slit2-Tg and wild-type mice. The effect of SLIT2 on inflammation, immune cell infiltration, M1 macrophage polarization, and alveolar bone loss in periodontitis was analyzed extensively. In periodontitis-affected gingival-tissue, SLIT2 expression was 4.4-fold higher compared to healthy-volunteers. LIP enhanced SLIT2 expression in mice periodontitis-affected periodontal tissue (PAPT) and blood circulation of wild-type mice by 4. 6-, and 5.0-fold, respectively. In Slit2-Tg-mice PAPT, SLIT2 expression was 1.8-fold higher compared to wild-type mice. Micro-CT and histomorphometric analysis revealed a 1.3-fold higher cement-enamel-junction to the alveolar-bone-crest (CEJ-ABC) distance and alveolar bone loss in LIP Slit2-Tg-mice compare to LIP wild-type mice. Results from RNA-sequencing, RT-qPCR, and ELISA showed a higher expression of Cxcr2, Il-18, TNFα, IL-6, and IL-1ß in Slit2-Tg-mice PAPT compared to wild-type-mice. Slit2-Tg-mice PAPT showed a higher number of osteoclasts, M1 macrophages, and the upregulation of Robo1 expression. Slit2-Tg-mice PAPT showed upregulation of M1 macrophage marker CD16/32 and osteoclastogenic markers Acp5, Ctsk, and Nfatc1, but osteogenic markers (Alp, Bglap) remained unchanged. Immunohistochemistry unveiled the higher vasculature and infiltration of leucocytes and macrophages in Slit2-Tg-mice PAPT. RNA-sequencing, GO-pathway enrichment analysis, and western blot analysis revealed the activation of the MAPK signaling pathway in Slit2-Tg mice PAPT. In conclusion, SLIT2 overexpression in periodontitis intensifies inflammation, immune cells infiltration, M1 macrophage polarization, osteoclastogenesis, and alveolar bone loss, possibly via activation of MAPK signaling, suggesting the role of SLIT2 on exacerbation of periodontitis and alveolar bone loss.

miR­543 acts as a novel oncogene in oral squamous cell carcinoma by targeting CYP3A5.

MicroRNAs (miRNAs/miRs) are small non­coding RNAs that can act as oncogenes or tumor­suppressor genes in human cancer. Previous studies have revealed that abnormal expression of miRNAs is closely associated with tumor cell cycle, differentiation, growth and apoptosis. miR­543 is expressed abnormally in a wide variety of cancers and has been associated with cellular proliferation, apoptosis, and invasion; however, the effect of miR­543 remains unknown in oral squamous cell carcinoma (OSCC). In the present study, the expression level of miR­543 in OSCC cell lines and tissues was investigated by RT­qPCR. A series of experiments was then performed to elucidate the functions of miR­543 in OSCC, such as CCK­8 assay, colony formation assay, flow cytometry, cell cycle distribution assay and cell apoptosis assay and Transwell assay. miR­543 expression was significantly upregulated in tumors from patients with OSCC and in OSCC cell lines. Overexpression of miR­543 promoted the proliferation, invasion and migration of OSCC cell lines, and inhibited cell apoptosis. In addition, the present study identified cytochrome P450 family 3 subfamily A member 5 (CYP3A5) as a direct target of miR­543 using software analysis and dual­luciferase reporter assays. In conclusion, the results of the present study suggest that miR­543 acts as a tumor promoter and serves a vital role in OSCC proliferation and invasion. These results confirm that miR­543 may serve as a potential novel target for the treatment of OSCC.

CircDOCK1 suppresses cell apoptosis via inhibition of miR­196a­5p by targeting BIRC3 in OSCC.

Oral squamous cell carcinoma (OSCC) is the most frequent oral cancer in the world, accounting for more than 90% of all oral cancer diagnosis. Circular RNAs (circRNAs) are large types of non-coding RNAs, demonstrating a great capacity of regulating the expression of genes. However, most of the functions of circRNAs are still unknown. Recent research revealed that circRNAs could serve as a miRNA-sponge, consequently regulating the expression of target genes indirectly, including oncogenes. In this study, we built an apoptotic model with TNF-α, and then we confirmed a circRNA associated with the apoptosis of OSCC cells, circDOCK1 by comparing the expression profile of circRNAs in an apoptotic model with that in untreated OSCC cells. We ascertained the presence of circDOCK1 with qRT­PCR and circRNA sequencing. The knockdown of the expression of circDOCK1 led to the increase of apoptosis. Utilizing multiple bioinformatics methods, we predicted the interactions among circRNAs, miRNAs and genes, and built the circDOCK1/miR­196a­5p/BIRC3 axis. Both the silencing of circDOCK1 with small interfering RNA and the upregulation of the expression of miR­196a­5p with mimics led OSCC cells to increase apoptosis and decrease BIRC3 formation. We further confirmed this outcome by comparing the expression of circDOCK1, miR­196a­5p and BIRC3 in oral squamous carcinoma tissue with those in para­carcinoma tissue, and examining the expression profile of circRNAs in oral squamous carcinoma tissue and para­carcinoma tissue with microarray. Our results demonstrated that circDOCK1 regulated BIRC3 expression by functioning as a competing endogenous RNA (ceRNA) and participated in the process of OSCC apoptosis. Thus, we propose that circDOCK1 could represent a novel potential biomarker and therapeutic target of OSCC.

TNF-α inhibits the migration of oral squamous cancer cells mediated by miR-765-EMP3-p66Shc axis.

Whereas TNF-α can facilitate the metastasis of oral squamous cancer cells (OSCC), whether it inhibits the metastasis is not clear so far. In this study, we demonstrated that high dose TNF-α at 100ng/mL could in vitro significantly inhibit the migration of two OSCC cell lines, CAL-27 and SCC-25. To explore the related mechanisms, we focused on the involvement of the microRNAs and found that TNF-α increased the expression of miR-765. The upregulation of miR-765 was attributed to the inhibition of the migration. We showed that miR-765 directly targeted EMP3 and suppressed its expression. We also found that the expression of EMP3 was much higher in human oral squamous cancer in compare with the surrounding normal tissue. Interestingly, p66Shc, a downstream molecule in the EMP3-related signaling pathway, was increased by TNF-α. We found that the overexpression of p66Shc could suppress the migration through the enhanced E-cadherin and ZO-1 signals. Either silencing the expression of EMP3 or enhancing the expression of miR-765 could upregulate the expression of p66Shc. Together, our results demonstrated that TNF-α inhibited the metastasis of oral squamous cancer cell through the miR-765-EMP3-p66Shc axis, which may provide new insights for the therapy of oral squamous cancer.

Control of a Wheelchair in an Indoor Environment Based on a Brain-Computer Interface and Automated Navigation.

The concept of controlling a wheelchair using brain signals is promising. However, the continuous control of a wheelchair based on unstable and noisy electroencephalogram signals is unreliable and generates a significant mental burden for the user. A feasible solution is to integrate a brain-computer interface (BCI) with automated navigation techniques. This paper presents a brain-controlled intelligent wheelchair with the capability of automatic navigation. Using an autonomous navigation system, candidate destinations and waypoints are automatically generated based on the existing environment. The user selects a destination using a motor imagery (MI)-based or P300-based BCI. According to the determined destination, the navigation system plans a short and safe path and navigates the wheelchair to the destination. During the movement of the wheelchair, the user can issue a stop command with the BCI. Using our system, the mental burden of the user can be substantially alleviated. Furthermore, our system can adapt to changes in the environment. Two experiments based on MI and P300 were conducted to demonstrate the effectiveness of our system.

An intelligent wheelchair based on automated navigation and BCI techniques.

In this paper, we propose an intelligent wheelchair system that relies on a brain computer interface (BCI) and automatic navigation. When in operation, candidate destinations and waypoints are automatically generated on the basis of the current environment. Then, the user selects a destination using a P300-based BCI. Finally, the navigation system plans a path and navigates the wheelchair to the determined destination. While the wheelchair is in motion, the user can issue a stop command with the BCI. Using our system, the mental burden of the user can be alleviated to a large degree. Furthermore, our system can adapt to changes in the environment. The experimental results demonstrated the effectiveness of our system.