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BACKGROUND: Ulcerative colitis (UC) is becoming a global burden. Previous observational studies have unveiled associations between serum metabolites and UC, but their causal relationship remains unclear. METHODS: Serum samples from patients and mice with UC were utilized for untargeted metabolomics to identify UC-associated metabolites. Then, a two-sample mendelian randomization (MR) analysis was employed to estimate their causal relationship. Finally, mice with chronic colitis induced by dextran sodium sulfate (DSS) and macrophages were used to evaluate the protective role of creatine and underlying mechanism. RESULTS: 16 serum metabolites showed associations with UC after adjusting for confounders and multiple testing. Among them, creatine exhibited a robust protective effect against UC (OR=0.39; 95 % CI=0.27-0.56). Significant reduction of creatine was also observed in mice with acute UC induced by DSS. The inverse variance weighted (IVW) MR analysis further confirmed a causal effect of creatine on UC risk (OR IVW=0.45; 95 % CI: 0.27-0.76). Furthermore, creatine supplementation could significantly suppress weight loss, disease activity index, mucosal damage and the infiltration of macrophages in mice with chronic colitis. Remarkably, creatine promoted the polarization of bone marrow-derived macrophage (BMDM) towards M2 phenotype and upregulated the expression of il-10, il-12 and arg-1. CONCLUSIONS: This study revealed a causal relationship between creatine and UC. Creatine supplementation ameliorated chronic colitis by inhibiting the colonic infiltration of macrophages and promoting its polarization towards M2 phenotype. These results offer new insight into the pathogenesis of UC, emphasizing a potential protective role of creatine for UC.

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Pentachlorophenol (PCP) was used widely as preservative and biocide and has been banned due to with various harmful effects, such as carcinogenicity and teratogenicity. However, the effects of PCP on colitis induced by dextrose sodium sulfate (DSS) remain largely unknown. Serum metabolomics and gut microbiota were investigated to elucidate the underlying mechanisms. Exposure to 20 µg/L PCP aggravated DSS-induced body weight loss, colon shortening, severe histological injuries, and upregulation of TNFα, iNOS, IL-1ß, and IL-6. Serum metabolomics showed that both DSS and PCP could significantly disrupted tryptophan metabolism in normal mice. Interestingly, PCP exposure intensified the disturbance in purine metabolism but not tryptophan metabolism caused by DSS. Quantitative analysis of tryptophan and metabolites further confirmed that PCP exposure significantly increased the serum contents of serotonin, adenine, guanine, guanosine, inosine monophosphate (IMP), inosine, and hypoxanthine in DSS-treated mice. The overall gut microbial community was significantly modified by PCP and DSS treatment alone. Rikenellaceae_RC9_Gut_group, Colidextribacter, and Desulfovibrio were more abundant in colitis mice following PCP exposure. Further integrative analysis of differential bacteria and purine metabolites highlighted a significant correlation between Desulfovibrio and several purine metabolites, including guanine, guanosine, hypoxanthine, IMP, and inosine. Adenosine ribonucleotides de novo biosynthesis, inosine-5'-phosphate biosynthesis I, and urate biosynthesis/inosine 5'-phosphate degradation pathways were depleted in colitis mice upon PCP treatment. Taken together, PCP exposure delayed the recovery of colitis induced by DSS in association with altered gut microbiota and serum metabolites, which were enriched in tryptophan and purine metabolism.

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AIMS: Vascular smooth muscle cell (VSMC) plasticity is a state in which VSMCs undergo phenotypic switching from a quiescent contractile phenotype into other functionally distinct phenotypes. Although emerging evidence suggest that VSMC plasticity plays critical roles in the development of vascular diseases, little is known about the key determinant for controlling VSMC plasticity and fate. METHODS AND RESULTS: We found that smooth muscle cell-specific deletion of Lkb1 in tamoxifen-inducible Lkb1flox/flox; Myh11-Cre/ERT2 mice spontaneously and progressively induced aortic/arterial dilation, aneurysm, rupture, and premature death. Single-cell RNA sequencing and imaging-based lineage tracing showed that Lkb1-deficient VSMCs transdifferentiated gradually from early modulated VSMCs to fibroblast-like and chondrocyte-like cells, leading to ossification and blood-vessel rupture. Mechanistically, Lkb1 regulates polypyrimidine tract binding protein 1 (Ptbp1) expression and controls alternative splicing of pyruvate kinase muscle (PKM) isoforms 1 and 2. Lkb1 loss in VSMC results in an increased PKM2/PKM1 ratio and alters the metabolic profile by promoting aerobic glycolysis. Treatment with PKM2 activator TEPP-46 rescues VSMC transformation and aortic dilation in Lkb1flox/flox; Myh11-Cre/ERT2 mice. Furthermore, we found that Lkb1 expression decreased in human aortic aneurysm tissue compared to control tissue, along with changes in markers of VSMC fate. CONCLUSIONS: Lkb1, via its regulation of Ptbp1-dependent alterative splicing of PKM, maintains VSMC in contractile states by suppressing VSMC plasticity.

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OBJECTIVE: Coronary artery ectasia (CAE) is a condition characterized by the localized or widespread dilation of one or more coronary arteries. The majority of CAE patients do not present with clinical symptoms, and the exact cause of CAE remains unclear. Therefore, a retrospective analysis was conducted to explore the potential causes of CAE. METHODS: This study was a retrospective analysis of patients who underwent coronary angiography at Guangdong Provincial People's Hospital between January 2017 and July 2022, of whom 679 patients were ultimately enrolled in the study. Among them, 260 patients were diagnosed with CAE, whereas 419 patients with normal coronary results composed the control group. Remnant cholesterol (RC) was calculated as total cholesterol (TC) minus high-density lipoprotein cholesterol (HDL-C) minus low-density lipoprotein cholesterol (LDL-C). The association between RC levels and the risk of CAE was assessed via multivariable logistic models. RESULTS: Out of the 679 patients who participated in this study, with an average age of 59.9 years, 38.3% were diagnosed with CAE. Patients with CAE had higher RC levels than did those without CAE (P = 0.001). A significant positive association was observed between RC levels and the risk of CAE, with a multivariable adjusted odds ratio (OR) of 1.950 (95% confidence interval [CI]: 1.163-3.270). There was a significant positive association between RC levels and the risk of CAE in both single-vessel and multivessel dilation cases, as well as in isolated CAE and dilation secondary to coronary atherosclerosis. According to the subgroup analyses, RC levels were positively associated with the risk of CAE in participants with hypertension (OR, 1.065; 95% CI, 1.034-1.098). CONCLUSION: RC levels are positively correlated with CAE, implying that a focus on RC could be beneficial in CAE research.

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Rehmannia piasezkii is a kind of medicinal plants, of the Orobanchaceae family, and well known for its large pink or purple corolla. However, no research on the molecular mechanism of flower color formation in R. piasezkii has been conducted so far. In this study, we investigated the transcriptome of root, stem, leaf and corollas of R. piasezkii using transcriptome sequencing technology and assembled 144,582 unigenes. A total of 58 anthocyanin biosynthetic genes were identified in the R. piasezkii transcriptome, fourteen of which were highly correlated with anthocyanin content, especially RpF3H2, RpDFR2, RpANS1, RpANS2 and RpUFGT. Totally, 35 MYB genes with FPKM values greater than 5 were identified in the R. piasezkii transcriptome, including an R2R3 MYB transcriptional factor RpMYB1, which belongs to subgroup 6 of the R2R3 MYB family. Agrobacterium-mediated transient expression of Nicotiana benthamiana revealed that overexpression of RpMYB1 could activate the expression of structural genes in anthocyanin synthesis pathway and promote the accumulation of anthocyanins in N. benthamiana leaves, indicating that RpMYB1 is a positive regulator of anthocyanin synthesis. Furthermore, combined transient overexpression of RpMYB1 with RpANS1, RpMYB1+RpANS1 with other structural genes all could further enhance the accumulation of anthocyanins in N. benthamiana leaves. Permanent overexpression of RpMYB1 in R. glutinosa promoted anthocyanin accumulation and expression levels of RgCHS, RgF3H, RgDFR and RgANS. Further evidence from dual-luciferase assay suggested that RpMYB1 could bind to the promoter of RpDFR2 and hence activating its expression. These findings provide insight into the molecular regulation in anthocyanin biosynthesis in R. piasezkii and provide valuable genetic resources for the genetic improvement of flower color.

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AIM: To compare relative peripheral refraction (RPR) in Chinese school children with different refractive errors using multispectral refraction topography (MRT). METHODS: A total of 713 eyes of primary school children [172 emmetropia (E), 429 low myopia (LM), 80 moderate myopia (MM), and 32 low hypermetropia (LH)] aged 10 to 13y were analyzed. RPRs were measured using MRT without mydriasis. MRT results showed RPR at 0-15° (RPR 0-15), 15°-30° (RPR 15-30), and 30°-45° (RPR 30-45) annular in the inferior (RPR-I), superior (RPR-S), nasal (RPR-N), and temporal (RPR-T) quadrants. Spherical equivalent (SE) was detected and calculated using an autorefractor. RESULTS: There were significant differences of RPR 15-30 between groups MM [0.02 (-0.12; 0.18)] and LH [-0.13 (-0.36; 0.12)] (P<0.05), MM and E [-0.06 (-0.20; 0.10)] (P<0.05), and LM [-0.02 (-0.15; 0.15)] and E (P<0.05). There were also significant differences of RPR 30-45 between groups MM [0.45 (0.18; 0.74)] and E [0.29 (-0.09; 0.67)] (P<0.05), and LM [0.44 (0.14; 0.76)] and E (P<0.001). RPR values increased from the hyperopic to medium myopic group in each annular. There were significant differences of RPR-S between groups MM [-0.02 (-0.60; 0.30)] and E [-0.44 (-0.89; -0.04)] (P<0.001), and LM [-0.28 (-0.71; 0.12)] and E (P<0.05). There were also significant differences of RPR-T between groups MM [0.37 (0.21; 0.78)] and LH [0.14 (-0.52; 0.50)] (P<0.05), LM [0.41 (0.06; 0.84)] and LH (P<0.05), and LM and E [0.29 (-0.10; 0.68), P<0.05]. A Spearman's correlation analysis showed a negative correlation between RPR and SE in the 15°-30° (P=0.005), 30°-45° (P<0.05) annular (P=0.002), superior (P<0.001), and temporal (P=0.001) quadrants. CONCLUSION: Without pupil dilation, values for RPR 15-30, 30-45, RPR-S, and T shows significant differences between myopic eyes and emmetropia, and the differences are negatively correlated with SE.

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BACKGROUND: Dexmedetomidine is a selective α2 receptor agonist with sedative, analgesic, anxiolytic, and anti-sympathetic effects. Dexmedetomidine is widely used for various surgical procedures performed under general anaesthesia and sedation in the intensive care unit. Dexmedetomidine was known to relieve or improve the symptoms of delirium. Schizophrenia is a common psychiatric disease, and the number of surgical patients with schizophrenia is increasing gradually. Dexmedetomidine-induced delirium in patients with schizophrenia is a particular case. CASE PRESENTATION: This patient was a 75-year-old woman (height: 156 cm; weight: 60 kg) with a 5-year history of schizophrenia. Her schizophrenia was well controlled with medications. She was scheduled for open reduction and internal fixation for a patellar fracture. Spinal anaesthesia was administered for surgery, and dexmedetomidine was administered intravenously to maintain sedation. The patient became delirious half an hour after the surgery began. The intravenous infusion of dexmedetomidine was discontinued immediately, intravenous propofol was subsequently administered, and the patient stopped experiencing dysphoria and fell asleep. After surgery, the patient stopped using propofol and recovered smoothly. She was transferred back to the general ward and was discharged from the hospital without any abnormal conditions on the 9th day after surgery. CONCLUSIONS: To the best of our knowledge, this is the first report of a patient with schizophrenia who developed delirium during the infusion of a normal dose of dexmedetomidine without an intravenous injection of any other sedative. The exact mechanism causing dexmedetomidine-induced delirium remains unclear, and this adverse reaction is rare and easy to ignore. Clinicians and pharmacists should be vigilant in identifying this condition.

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[This retracts the article DOI: 10.3892/ol.2019.9978.].

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PURPOSE: The purpose of this study was to compare the effect of ultrasound-guided continuous erector spinae plane block to continuous thoracic paravertebral block on postoperative analgesia in elderly patients who underwent thoracoscopic lobectomy. DESIGN: Randomized controlled trial. METHODS: Elderly patients (N = 50) who underwent nonemergent thoracoscopic lobectomy in the thoracic surgery department of our hospital from January 2019 to December 2020 were selected and randomly divided into continuous erector spinae block (ESPB; n = 25) group and continuous thoracic paravertebral block (TPVB; n = 25) group. The patients in the two groups were guided by ultrasound with ESPB or TPVB before anesthesia induction. The visual analog scale at rest and cough in 2 hours, 6 hours, 8 hours, 12 hours, 24 hours, 48 hours after surgery, the supplementary analgesic dosage of tramadol, time of tube placement, the stay time in postanesthesia care unit (PACU), the first ambulation time after surgery, the length of postoperative hospital stay and postoperative complications were recorded. FINDINGS: There were no significant differences between the two groups in visual analog scale score at rest and cough at each time point and supplementary analgesic dosage of tramadol within 48 hours after surgery (P > .05). The time of tube placement and the postoperative hospital stay in ESPB group was significantly shorter than that in TPVB group (P < .05). There were no differences in PACU residence time and first ambulation time between the two groups (P > .05). There were 4 patients in TPVB group and 2 patients in ESPB group who had nausea and vomiting (P > .05), 1 case of pneumothorax and 1 case of fever in the TPVB group. There were no incision infections or respiratory depression requiring clinical intervention in either group. CONCLUSIONS: Both ESPB and TPVB alleviated the patients postoperative pain effectively for elderly patients underwent thoracoscopic lobectomy. Compared with TPVB, patients with ESPB have a shorter tube placement time, fewer complications and faster postoperative recovery.

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Equine influenza (EI) is a severe infectious disease that causes huge economic losses to the horse industry. Spatial epidemiology technology can explore the spatiotemporal distribution characteristics and occurrence risks of infectious diseases, it has played an important role in the prevention and control of major infectious diseases in humans and animals. For the first time, this study conducted a systematic analysis of the spatiotemporal distribution of EI using SaTScan software and investigated the important environmental variables and suitable areas for EI occurrence using the Maxent model. A total of 517 occurrences of EI from 2005 to 2022 were evaluated, and 14 significant spatiotemporal clusters were identified. Furthermore, a Maxent model was successfully established with high prediction accuracy (AUC = 0.920 ± 0.008). The results indicated that annual average ultraviolet radiation, horse density, and precipitation of the coldest quarter were the three most important environmental variables affecting EI occurrence. The suitable areas for EI occurrence are widely distributed across all continents, especially in Asia (India, Mongolia, and China) and the Americas (Brazil, Uruguay, USA, and Mexico). In the future, these suitable areas will expand and move eastward. The largest expansion is predicted under SSP126 scenarios, while the opposite trend will be observed under SSP585 scenarios. This study presents the spatial epidemiological characteristics of EI for the first time. The results could provide valuable scientific insights that can effectively inform prevention and control strategies in regions at risk of EI worldwide.

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PURPOSE: To analyze the hotspots and trends in artificial intelligence (AI) research in the field of cataracts. METHODS: The Science Citation Index Expanded of the Web of Science Core Collection was used to collect the research literature related to AI in the field of cataracts, which was analyzed for valuable information such as years, countries/regions, journals, institutions, citations, and keywords. Visualized co-occurrence network graphs were generated through the library online analysis platform, VOSviewer, and CiteSpace tools. RESULTS: A total of 222 relevant research articles from 41 countries were selected. Since 2019, the number of related articles has increased significantly every year. China (n = 82, 24.92%), the United States (n = 55, 16.72%) and India (n = 26, 7.90%) were the three countries with the most publications, accounting for 49.54% of the total. The Journal of Cataract and Refractive Surgery (n = 13, 5.86%) and Translational Vision Science & Technology (n = 10, 4.50%) had the most publications. Sun Yat-sen University (n = 25, 11.26%), the Chinese Academy of Sciences (n = 17, 7.66%), and Capital Medical University (n = 16, 7.21%) are the three institutions with the highest number of publications. We discovered through keyword analysis that cataract, diagnosis, imaging, classification, intraocular lens, and formula are the main topics of current study. CONCLUSIONS: This study revealed the hot spots and potential trends of AI in terms of cataract diagnosis and intraocular lens power calculation. AI will become more prevalent in the field of ophthalmology in the future.

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Host-directed therapy (HDT) is a new adjuvant strategy that interfere with host cell factors that are required by a pathogen for replication or persistence. In this study, we assessed the effect of dehydrozaluzanin C-derivative (DHZD), a modified compound from dehydrozaluzanin C (DHZC), as a potential HDT agent for severe infection. LPS-induced septic mouse model and Carbapenem resistant Klebsiella pneumoniae (CRKP) infection mouse model was used for testing in vivo. RAW264.7 cells, mouse primary macrophages, and DCs were used for in vitro experiments. Dexamethasone (DXM) was used as a positive control agent. DHZD ameliorated tissue damage (lung, kidney, and liver) and excessive inflammatory response induced by LPS or CRKP infection in mice. Also, DHZD improved the hypothermic symptoms of acute peritonitis induced by CRKP, inhibited heat-killed CRKP (HK-CRKP)-induced inflammatory response in macrophages, and upregulated the proportions of phagocytic cell types in lungs. In vitro data suggested that DHZD decreases LPS-stimulated expression of IL-6, TNF-α and MCP-1 via PI3K/Akt/p70S6K signaling pathway in macrophages. Interestingly, the combined treatment group of DXM and DHZD had a higher survival rate and lower level of IL-6 than those of the DXM-treated group; the combination of DHZD and DXM played a synergistic role in decreasing IL-6 secretion in sera. Moreover, the phagocytic receptor CD36 was increased by DHZD in macrophages, which was accompanied by increased bacterial phagocytosis in a clathrin- and actin-dependent manner. This data suggests that DHZD may be a potential drug candidate for treating bacterial infections.

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The Steady-State Visual Evoked Potential (SSVEP) is a widely used modality in Brain-Computer Interfaces (BCIs). Existing research has demonstrated the capabilities of SSVEP that use single frequencies for each target in various applications with relatively small numbers of commands required in the BCI. Multi-frequency SSVEP has been developed to extend the capability of single-frequency SSVEP to tasks that involve large numbers of commands. However, the development on multi-frequency SSVEP methodologies is falling behind compared to the number of studies with single-frequency SSVEP. This dataset was constructed to promote research in multi-frequency SSVEP by making SSVEP signals collected with different frequency stimulation settings publicly available. In this dataset, SSVEPs were collected from 35 participants using single-, dual-, and tri-frequency stimulation and with three different multi-frequency stimulation variants.

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Non-alcoholic fatty liver disease (NAFLD) has become a serious public health issue due to changing dietary patterns and composition. However, the relationship between NAFLD occurrence and food additives, such as preservatives, remains unknown. This study aimed to evaluate the toxicity of parabens, namely methylparaben (MeP) and ethylparaben (EtP), in relation to NAFLD occurrence in mice under different dietary conditions. Exposure to MeP and EtP exacerbated high-fat diet (HFD)-induced obesity, glucose intolerance, higher serum lipid concentrations, and fat accumulation by upregulating genes involved in lipid metabolism. Untargeted metabolomics revealed that arachidonic acid (AA) metabolism was the top enriched pathway upon MeP and EtP exposure in the presence of HFD. 11,12-Epoxyeicosatrienoic acid (11,12-EET) was the most abundant AA metabolite and was significantly reduced upon exposure to MeP or EtP. Moreover, an integrative analysis of differential fecal taxa at the genus level and serum AA metabolites revealed significant associations. In addition, MeP and EtP enhanced lipid accumulation in AML12 cells and HepG2 cells cultured with oleic acid. 11,12-EET supplementation could significantly alleviate lipid accumulation by suppressing the expression of lipid metabolism-related genes and proteins. The present study suggests that chronic exposure to MeP and EtP promoted NAFLD via gut microbiota-dependent AA metabolism. These results highlight the need for reducing oral exposure to synthetic preservatives to improve metabolic disturbance under HFD conditions.

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AIM: Intussusception is the most common surgical complication of IgA vasculitis (IgAV), and intestinal perforation is usually associated with intussusception. If they are not recognised and treated in a timely manner, serious consequences may occur. The objective is to summarise the clinical features of IgAV complicated by intussusception and intestinal perforation and explore its risk factors. METHODS: The clinical data of 32 patients with IgAV complicated by surgical complications (25 cases of intussusception and 7 cases of intestinal perforation) were retrospectively analysed. A total of 160 IgAV children with gastrointestinal (GI) involvement but without surgical complications were randomly selected as a control group. Binary logistic regression analysis was performed to explore the risk factors for IgAV with intussusception and intestinal perforation. RESULTS: Compared with the intussusception group, the intestinal perforation group had a significantly higher number of patients with GI symptoms prior to skin purpura and GI bleeding, a significantly higher number of days of abdominal pain, a significantly higher Wong-Baker score, and a significantly higher white blood cell count. Multivariate logistic regression analysis indicated that age ≤7 years, GI symptoms prior to skin purpura, abdominal pain intensity (Wong-Baker scale) and timing of glucocorticoid treatment were independent risk factors of IgAV with intussusception and intestinal perforation. CONCLUSION: Age less than 7 years, severe abdominal pain, and GI symptoms prior to skin purpura were risk factors for IgAV with intussusception and intestinal perforation. Early use of glucocorticoids may prevent intussusception and intestinal perforation.

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PYCARD (PYD and CARD domain containing), a pivotal adaptor protein in inflammasome assembly and activation, contributes to innate immunity, and plays an essential role in the pathogenesis of atherosclerosis and restenosis. However, its roles in microRNA biogenesis remain unknown. Therefore, this study aimed to investigate the roles of PYCARD in miRNA biogenesis and neointima formation using pycard knockout (pycard-/-) mice. Deficiency of Pycard reduced circulating miRNA profile and inhibited Mir17 seed family maturation. The systemic pycard knockout also selectively reduced the expression of AGO2 (argonaute RISC catalytic subunit 2), an important enzyme in regulating miRNA biogenesis, by promoting chaperone-mediated autophagy (CMA)-mediated degradation of AGO2, specifically in adipose tissue. Mechanistically, pycard knockout increased PRMT8 (protein arginine N-methyltransferase 8) expression in adipose tissue, which enhanced AGO2 methylation, and subsequently promoted its binding to HSPA8 (heat shock protein family A (Hsp70) member 8) that targeted AGO2 for lysosome degradation through chaperone-mediated autophagy. Finally, the reduction of AGO2 and Mir17 family expression prevented vascular injury-induced neointima formation in Pycard-deficient conditions. Overexpression of AGO2 or administration of mimic of Mir106b (a major member of the Mir17 family) prevented Pycard deficiency-mediated inhibition of neointima formation in response to vascular injury. These data demonstrate that PYCARD inhibits CMA-mediated degradation of AGO2, which promotes microRNA maturation, thereby playing a critical role in regulating neointima formation in response to vascular injury independently of inflammasome activity and suggest that modulating PYCARD expression and function may represent a powerful therapeutic strategy for neointima formation.Abbreviations: 6-AN: 6-aminonicotinamide; ACTB: actin, beta; aDMA: asymmetric dimethylarginine; AGO2: argonaute RISC catalytic subunit 2; CAL: carotid artery ligation; CALCOCO2: calcium binding and coiled-coil domain 2; CMA: chaperone-mediated autophagy; CTSB: cathepsin B; CTSD: cathepsin D; DGCR8: DGCR8 microprocessor complex subunit; DOCK2: dedicator of cyto-kinesis 2; EpiAdi: epididymal adipose tissue; HSPA8: heat shock protein family A (Hsp70) member 8; IHC: immunohistochemical; ISR: in-stent restenosis; KO: knockout; LAMP2: lysosomal-associated membrane protein 2; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; miRNA: microRNA; NLRP3: NLR family pyrin domain containing 3; N/L: ammonium chloride combined with leupeptin; PRMT: protein arginine methyltransferase; PVAT: peri-vascular adipose tissues; PYCARD: PYD and CARD domain containing; sDMA: symmetric dimethylarginine; ULK1: unc-51 like kinase 1; VSMCs: vascular smooth muscle cells; WT: wild-type.

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Recent advances in wearable ultrasound technologies have demonstrated the potential for hands-free data acquisition, but technical barriers remain as these probes require wire connections, can lose track of moving targets and create data-interpretation challenges. Here we report a fully integrated autonomous wearable ultrasonic-system-on-patch (USoP). A miniaturized flexible control circuit is designed to interface with an ultrasound transducer array for signal pre-conditioning and wireless data communication. Machine learning is used to track moving tissue targets and assist the data interpretation. We demonstrate that the USoP allows continuous tracking of physiological signals from tissues as deep as 164 mm. On mobile subjects, the USoP can continuously monitor physiological signals, including central blood pressure, heart rate and cardiac output, for as long as 12 h. This result enables continuous autonomous surveillance of deep tissue signals toward the internet-of-medical-things.

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Low decoding accuracy makes brain-computer interface (BCI) control of a robotic arm difficult. Shared control (SC) can overcome limitations of a BCI by leveraging external sensor data and generating commands to assist the user. Our study explored whether reaching targets with a robot end-effector was easier using SC rather than direct control (DC). We simulated a motor imagery BCI using a joystick with noise introduced to explicitly control interface accuracy to be 65% or 79%. Compared to DC, our prediction-based implementation of SC led to a significant reduction in the trajectory length of successful reaches for 4 (3) out of 5 targets using the 65% (79%) accurate interface, with failure rates being equivalent to DC for 2 (1) out of 5 targets. Therefore, this implementation of SC is likely to improve reaching efficiency but at the cost of more failures. Additionally, the NASA Task Load Index results suggest SC reduced user workload.Clinical relevance-Shared control can minimise the impact of BCI decoder errors on robot motion, making robotic arm control using noninvasive BCIs more viable.

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Multi-frequency steady-state visual evoked potential (SSVEP) aims to increase the number of targets in SSVEP-based brain-computer interfaces. However, the effectiveness of multi-frequency SSVEP when there is a large number of targets compared to traditional single-frequency SSVEP has not been demonstrated to date. It is also unclear the degree to which multi-frequency SSVEP outperforms single-frequency SSVEP as the number of targets increases. This study directly compares single-frequency and dual-frequency SSVEPs for different numbers of targets within a fixed (5 Hz) frequency range. Our results demonstrate that dual-frequency SSVEP maintains its performance at a high level of accuracy in the range while single-frequency SSVEP performance falls as the number of targets becomes very high within the given frequency range. In this particular study, dual-frequency SSVEP has a clear advantage when there are more than 120 targets in a 5 Hz frequency range.

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