Interfacial Cherenkov radiation from ultralow-energy electrons.

Cherenkov radiation occurs only when a charged particle moves with a velocity exceeding the phase velocity of light in that matter. This radiation mechanism creates directional light emission at a wide range of frequencies and could facilitate the development of on-chip light sources except for the hard-to-satisfy requirement for high-energy particles. Creating Cherenkov radiation from low-energy electrons that has no momentum mismatch with light in free space is still a long-standing challenge. Here, we report a mechanism to overcome this challenge by exploiting a combined effect of interfacial Cherenkov radiation and umklapp scattering, namely the constructive interference of light emission from sequential particle-interface interactions with specially designed (umklapp) momentum-shifts. We find that this combined effect is able to create the interfacial Cherenkov radiation from ultralow-energy electrons, with kinetic energies down to the electron-volt scale. Due to the umklapp scattering for the excited high-momentum Bloch modes, the resulting interfacial Cherenkov radiation is uniquely featured with spatially separated apexes for its wave cone and group cone.

Fe3 C/nanocarbon-Enabled Lithium Dendrite Mitigation in Lithium-Sulfur batteries.

Lithium dendrite-induced short circuits and material loss are two major obstacles to the commercialization of lithium-sulfur (Li-S) batteries. Here, a nanocarbon composite consisting of cotton-derived Fe3 C-encapsulated multiwalled carbon nanotubes (Fe3 C-MWCNTs) and graphene effectively traps polysulfides to suppress lithium dendrite growth is reported. Machine learning combined with molecular dynamics (MD) simulations unveils a new polysulfide-induced lithium dendrite formation mechanism: the migration of polysulfides away from the anode drags out lithium protrusions through localized lattice distortion of the lithium anode and traps lithium ions in the surrounding electrolyte, leading to lithium dendrite formation. The Li-S battery, constructed using the composite of cotton-derived Fe3 C-MWCNTs and graphene that serves as both the sulfur host and the anode interlayer, exhibits exceptional cycling stability, impressive capacity retention, and effective mitigation of lithium dendrite formation. The findings offer valuable strategies to prevent lithium dendrite formation and enhance understanding of lithium dendrite growth in Li-S batteries.

Low-Velocity-Favored Transition Radiation.

When a charged particle penetrates through an optical interface, photon emissions emerge-a phenomenon known as transition radiation. Being paramount to fundamental physics, transition radiation has enabled many applications from high-energy particle identification to novel light sources. A rule of thumb in transition radiation is that the radiation intensity generally decreases with the decrease of particle velocity v; as a result, low-energy particles are not favored in practice. Here, we find that there exist situations where transition radiation from particles with extremely low velocities (e.g., v/c<10^{-3}) exhibits comparable intensity as that from high-energy particles (e.g., v/c=0.999), where c is the light speed in free space. The comparable radiation intensity implies an extremely high photon extraction efficiency from low-energy particles, up to 8 orders of magnitude larger than that from high-energy particles. This exotic phenomenon of low-velocity-favored transition radiation originates from the interference of the excited Ferrell-Berreman modes in an ultrathin epsilon-near-zero slab. Our findings may provide a promising route toward the design of integrated light sources based on low-energy electrons and specialized detectors for beyond-standard-model particles.

Cotton-Derived Fe/Fe3C-Encapsulated Carbon Nanotubes for High-Performance Lithium-Sulfur Batteries.

Fabrication processes of fossil fuel-derived carbon nanomaterials are of high carbon emissions. Deriving carbon materials from low-cost and sustainable biomass is eco-friendly. Cotton, one of the most abundant biomass materials, naturally holds a hierarchically porous structure, making the activated cotton textile (ACT) an ideal scaffold for loading active materials. Here, we report a low-cost approach to massively producing multiwalled carbon nanotubes (MWCNTs) via a combination process of vapor-liquid-solid (VLS) and solid-liquid-solid (SLS) where cotton decomposed into carbon-containing gases and amorphous carbons that then dissolved into Fe nanoparticles, forming Fe/Fe3C-encapsulated MWCNTs. The lithium-sulfur (Li-S) battery constructed by the Fe/Fe3C-MWCNT@ACT/S composite (as the cathode) and the Fe/Fe3C-MWCNT@ACT (as the interlayer) exhibited a superlative cycling stability (over 1000 cycles at 1.0 C), an ultralow capacity decay rate (0.0496% per cycle) and a remarkable specific capacity (1273 mAh g-1 at 0.1 C). The Fe/Fe3C-MWCNTs enhanced electrode stability and suppressed polysulfide dissolution during cycling.

Social support as a protective factor against the effect of grief reactions on depression for bereaved single older adults.

This study tested the main effect model and the stress-buffering model of the mechanisms by which social support affects bereaved single older adults' depression. Data from the National Social Life, Health, and Aging Project (Wave 2; N = 621) were used to test a latent moderated structural equation model that explores the interaction between grief reactions and social support on bereaved single older adults' depression in the US. The findings provide evidence for the stress-buffering model (i.e., the relationship between grief reactions and depression, which was strongly positive when social support was low, turned negative when social support was high).

Polymorphisms in MicroRNA Target Sites of TGF-ß Signaling Pathway Genes and Susceptibility to Allergic Rhinitis.

BACKGROUND: The polymorphisms inside microRNA target sites locating in the 3'-UTR region may introduce the micro-RNA-binding changes, which may regulate the gene expression and correlate with the potential diseases. OBJECTIVES: We aimed to investigate whether the polymorphisms in microRNA target sites of transforming growth factor beta (TGF-ß) signaling pathway genes are associated with the susceptibility of mite-sensitized allergic rhinitis (AR) in a Han Chinese population. METHODS: In this case-control study, 454 AR patients and 448 healthy controls were recruited. Three HapMap single-nucleotide polymorphisms (SNPs) were mapped to putative microRNA recognition sites and genotyped by TaqMan allelic discrimination assay. RESULTS: The genotype and allele frequencies of 3 SNPs (rs1590 in TGFBR1; rs1434536 and rs17023107 in BMPR1B) showed lack of significant association with AR. However, in the subgroup analysis, the TG, GG, and TG/GG genotypes of rs1590 exhibited significantly increased risk of AR in the male subgroup (TG: adjusted OR = 1.57, 95% CI = 1.08-2.31; GG: adjusted OR = 1.76, 95% CI = 1.09-2.86; TG/GG: adjusted OR = 1.62, 95% CI = 1.13-2.33). The CT genotypes of rs17023107 might have potential to protect against AR in the patients age of <15 years (adjusted OR = 0.37, 95% CI = 0.14-0.95) and the males (adjusted OR = 0.48, 95% CI = 0.25-0.95). No significant association was found between SNPs and the total serum IgE level. CONCLUSIONS: In a Han Chinese population, stratified by age and gender, susceptibility to mite-sensitized AR may be associated with 2 SNPs (rs1590 and rs17023107) in microRNA target sites of TGF-ß signaling pathway genes.

Lithiation-Aided Conversion of End-of-Life Lithium-Ion Battery Anodes to High-Quality Graphene and Graphene Oxide.

In the past two decades, lithium-ion (Li-ion) batteries have transformed the appearance of the world. Along with the ever-increasing production and usage are the tremendous number of retired batteries, which have created social and environmental issues, making battery recycling an urgent task. Graphene has exhibited outstanding electronic and mechanical properties but it is still difficult to fabricate high-quality graphene with feasible procedures at low cost. Here, a strategy of smartly converting retired Li-ion battery anodes to graphene and graphene oxide is proposed. The graphite powders collected from end-of-life Li-ion batteries exhibited irregular expansion because of the lithium-ion intercalation and deintercalation in the anodegraphite during battery charge/discharge. Such prefabrication process facilitated both chemical and physical exfoliations of the graphite. Comparing with the graphene oxide derived from pristine, untreated graphite, the graphene oxide from anodegraphite exhibited superlative homogeneity and electrochemical properties. The lithiation aided pre-expansion enabled 4 times enhancement of graphene productivity by shear mixing. Furthermore, the graphene fabrication was seamlessly inserted into the currently used battery recycling streamline in which the acid treatment was found to further swell the graphite lattice, pushing up the graphene productivity to 83.7% (10 times higher than that of pristine graphite powders). The findings create new opportunities for capitalizing on waste batteries to produce high-quality graphene and its derivatives.

The Virulence Function and Regulation of the Metalloprotease Gene prtA in the Plant-Pathogenic Bacterium Burkholderia glumae.

Bacterial panicle blight caused by Burkholderia glumae is a major bacterial disease of rice. Our preliminary RNA-seq study showed that a serine metalloprotease gene, prtA, is regulated in a similar manner to the genes for the biosynthesis and transport of toxoflavin, which is a known major virulence factor of B. glumae. prtA null mutants of the virulent strain B. glumae 336gr-1 did not show a detectable extracellular protease activity, indicating that prtA is the solely responsible gene for the extracellular protease activity detected from this bacterium. In addition, inoculation of rice panicles with the prtA mutants resulted in a significant reduction of disease severity compared with the wild-type parent strain, suggesting the requirement of prtA for the full virulence of B. glumae. A double mutant deficient in both serine metalloprotease and toxoflavin (ΔtoxA/prtA-) exhibited a further numeric but not statistically significant decrease of disease development compared with the ΔtoxA strain. Both the prtA-driven extracellular protease activity and the toxoflavin production were dependent on both the tofI/tofR quorum-sensing and the global regulatory gene qsmR, indicating the important roles of the two global regulatory factors for the bacterial pathogenesis by this pathogen.

Identification of new regulatory genes involved in the pathogenic functions of the rice-pathogenic bacterium Burkholderia glumae.

Burkholderia glumae is an emerging plant-pathogenic bacterium that causes disease in rice in several of the major rice-producing areas throughout the world. In the southern United States, B. glumae is the major causal agent of bacterial panicle blight of rice and has caused severe yield losses in recent decades. Despite its importance, few management options are available for diseases caused by B. glumae, and knowledge of how this pathogen causes disease is limited. In an effort to identify novel factors that contribute to the pathogenicity of B. glumae, random mutagenesis using the miniTn5gus transposon was performed on two strains of B. glumae. Resultant mutants were screened in the laboratory for altered phenotypes in various known or putative virulence factors, including toxoflavin, lipase and extracellular polysaccharides. Mutants that exhibited altered phenotypes compared to their parent strain were selected and subsequently characterized using a PCR-based method to identify the approximate location of the transposon insertion. Altogether, approximately 20 000 random mutants were screened and 51 different genes were identified as having potential involvement in the production of toxoflavin, lipase and/or extracellular polysaccharide. Especially, two regulatory genes, ntpR and tepR, encoding a LysR-type transcriptional regulator and a σ54-dependent response regulator, respectively, were discovered in this study as new negative regulatory factors for the production of toxoflavin, the major phytotoxin synthesized by B. glumae and involved in bacterial pathogenesis.

Association of systemic inflammation index with psoriasis risk and psoriasis severity: A retrospective cohort study of NHANES 2009 to 2014.

To investigate the association of systemic inflammation index (SII) with psoriasis risk and psoriasis severity. This is a retrospective cohort study based on data from the National Health and Nutrition Examination Survey database from 2009 to 2014. The psoriasis information was obtained from the questionnaire data, and the SII was calculated as neutrophil × platelet/lymphocyte. We performed matching by controlling age and gender to reach a 1:2 ratio for better statistical power. Weighted logistic regression analysis, subgroup analysis, restricted cubic spline analysis, and threshold analysis were used to evaluate the association of SII with psoriasis risk. Besides, mediation analysis was conducted to assess the possible regulatory path. Finally, the receiver operating characteristic curve was plotted to analyze the predictive value of SII for psoriasis severity. The study involved 16,466 participants including 16,020 no-psoriasis participants and 446 psoriasis participants. After matching, psoriasis and non-psoriasis individuals were 446 and 892, respectively. SII was significantly higher in the psoriasis group than the non-psoriasis group (P < .05). Additionally, white blood cells and monocytes were significantly linked to psoriasis risk and SII scores (P < .05). Besides, SII elevation was an independent predictor for upregulated psoriasis risk (P < .05). There was a nonlinear relationship between SII and psoriasis risk (P nonlinear < .05), which was not mediated by white blood cells and monocytes. Unexpectedly, SII had no significance in predicting SII severity (P > .05). SII can independently predict psoriasis risk but has no impact on psoriasis severity. Further, SII serves as a potential and robust biomarker for identifying high-risk psoriasis individuals.

Estimating the Heterogeneous Causal Effects of Parent-Child Relationships among Chinese Children with Oppositional Defiant Symptoms: A Machine Learning Approach.

Oppositional defiant symptoms are some of the most common developmental symptoms in children and adolescents with and without oppositional defiant disorder. Research has addressed the close association of the parent-child relationship (PCR) with oppositional defiant symptoms. However, it is necessary to further investigate the underlying mechanism for forming targeted intervention strategies. By using a machine learning-based causal forest (CF) model, we investigated the heterogeneous causal effects of the PCR on oppositional defiant symptoms in children in Chinese elementary schools. Based on the PCR improvement in two consecutive years, 423 children were divided into improved and control groups. The assessment of oppositional defiant symptoms (AODS) in the second year was set as the dependent variable. Additionally, several factors based on the multilevel family model and the baseline AODS in the first year were included as covariates. Consistent with expectations, the CF model showed a significant causal effect between the PCR and oppositional defiant symptoms in the samples. Moreover, the causality exhibited heterogeneity. The causal effect was greater in those children with higher baseline AODS, a worse family atmosphere, and lower emotion regulation abilities in themselves or their parents. Conversely, the parenting style played a positive role in causality. These findings enhance our understanding of how the PCR contributes to the development of oppositional defiant symptoms conditioned by factors from a multilevel family system. The heterogeneous causality in the observation data, established using the machine learning approach, could be helpful in forming personalized family-oriented intervention strategies for children with oppositional defiant symptoms.

Free-electron Brewster-transition radiation.

We reveal a mechanism to enhance particle-matter interactions by exploiting the pseudo-Brewster effect of gain materials, presenting an enhancement of at least four orders of magnitude for light emission. This mechanism is enabled by the emergence of an unprecedented phase diagram that maps all phenomena of free-electron transition radiation into three distinct phases in a gain-thickness parameter space, namely, the conventional, intermediate, and Brewster phases, when an electron penetrates a dielectric slab with a modest gain and a finite thickness. Essentially, our revealed mechanism corresponds to the free-electron transition radiation in the Brewster phase, which also features ultrahigh directionality, always at the Brewster angle, regardless of the electron velocity. Counterintuitively, we find that the intensity of this free-electron Brewster-transition radiation is insensitive to the Fabry-Pérot resonance condition and, thus, the variation of slab thickness, and moreover, a weaker gain could lead to a stronger enhancement for light emission.

Corrigendum: The m6A-methylated mRNA pattern and the activation of the Wnt signaling pathway under the hyper-m6A-modifying condition in the keloid.

[This corrects the article DOI: 10.3389/fcell.2022.947337.].

[Effects of Astragalus polysaccharide on imiquimod-induced psoriasiform dermatitis in mice and its mechanisms].

Objective: To investigate the effects and mechanisms of Astragalus polysaccharide on improving imiquimod-induced psoriasiform dermatitis in mice. Methods: Forty healthy female C57BL/6 mice were randomly divided into 5 groups, including blank control group, model group, astragalus polysaccharide high-dose group (200 mg/kg), medium-dose group (100 mg/kg) and low-dose group (50 mg/kg), with 8 mice in each group. The mice in model group and astragalus polysaccharide treatment group were treated with 5% imiquimod cream on the back to induce psoriasiform dermatitis. PASI score was monitored, and the secretion of inflammatory factors was determined by ELISA. The secretion of inflammatory factors was closely related to the infiltration of macrophages. The infiltration of macrophages in skin was detected by flow cytometry to further explore the effect of different concentrations of APS on psoriasis. Results: Compared with control group, the PASI score and the serum levels of TNF-α, IL-1ß and IL-6 were increased significantly (P＜0.05), and the infiltration of macrophages in skin tissue was increased significantly in model group (P＜0.05). Compared with model group, the PASI score was decreased significantly (P＜0.05), and the serum levels of TNF-α, IL-1ß and IL-6 were down-regulated significantly in astragalus polysaccharide high-dose and medium-dose groups (P＜0.05). The infiltrating macrophages in skin tissue were decreased significantly in Astragalus polysaccharide high-dose group (P＜0.05). Conclusion: Astragalus polysaccharide improve psoriasiform dermatitis in mice by inhibiting the infiltration of macrophages in skin tissue and decreasing the secretion of TNF-α, IL-1ß and IL-6 in serum.

TLR Signaling Pathway Gene Polymorphisms, Gene-Gene and Gene-Environment Interactions in Allergic Rhinitis.

Background: Allergic rhinitis (AR) is a nasal inflammatory disease resulting from a complex interplay between genetic and environmental factors. The association between Toll-like receptor (TLR) signaling pathway and environmental factors in AR pathogenesis remains to be explored. This study aims to assess the genetic association of AR with single nucleotide polymorphisms (SNPs) in TLR signaling pathway, and investigate the roles of gene-gene and gene-environment interactions in AR. Methods: A total of 452 AR patients and 495 healthy controls from eastern China were enrolled in this hospital-based case-control study. We evaluated putatively functional genetic polymorphisms in TLR2, TLR4 and CD14 genes for their association with susceptibility to AR and related clinical phenotypes. Interactions between environmental factors (such as traffic pollution, residence, pet keeping) and polymorphisms with AR were examined using logistic regression. Models were stratified by genotype and interaction terms, and tested for the significance of gene-gene and gene-environment interactions. Results: In the single-locus analysis, two SNPs in CD14, rs2563298 (A/C) and rs2569191 (C/T) were associated with a significantly decreased risk of AR. Compared with the GG genotype, the GT and GT/TT genotypes of TLR2 rs7656411 (G/T) were associated with a significantly increased risk of AR. Gene-gene interactions (eg, TLR2 rs7656411, TLR4 rs1927914, and CD14 rs2563298) was associated with AR. Gene-environment interactions (eg, TLR4 or CD14 polymorphisms and certain environmental exposures) were found in AR cases, but they were not significant after Bonferroni correction. Conclusion: The genetic polymorphisms of TLR2 and CD14 and gene-gene interactions in TLR signaling pathway were associated with susceptibility to AR in this Han Chinese population. However, the present results were limited to support the association between gene-environment interactions and AR.

GARP Polymorphisms Associated with Susceptibility to House Dust Mite-Sensitized Persistent Allergic Rhinitis in a Chinese Population.

Background: Genetic variants in GARP (also known as LRRC32) have been reported to have significant associations with asthma and eczema in special populations, but little is known about allergic rhinitis. This study purposes to evaluate the association of single nucleotide polymorphisms (SNPs) in GARP with house dust mite (HDM)-sensitized persistent allergic rhinitis (PER) in a population of Han Chinese. Methods: In this hospital-based case-control study, 534 HDM-sensitized PER patients and 451 healthy controls were recruited from East China. In this population, six SNPs in GARP were identified. Serum total and specific IgE levels were measured with ImmunoCAP. Secondary structure and minimum free energy were predicted by RNAfold. Results: rs79525962 was associated with the risk of HDM-sensitized PER (P < 0.05). The individuals with CT+TT genotype demonstrated a higher risk of HDM-sensitized PER than those with CC genotype (adjusted OR = 1.393, 95% CI = 1.019-1.904). The homozygous genotype CC of rs3781699 rendered a lower risk of HDM-sensitized PER than the wild-type genotype AA (adjusted OR = 0.646, 95% CI = 0.427-0.976); however, the genotype and allele frequencies of rs3781699 demonstrated no associations with HDM-sensitized PER (P > 0.05). rs79525962 increased the risk of HDM-sensitized PER in the subgroup aged ≥16 years (adjusted OR = 1.745, 95% CI = 1.103-2.760), and this high risk was also found in the females (adjusted OR = 1.708, 95% CI = 1.021-2.856). The G-C haplotype of rs1320646-rs3781699 rendered a lower risk of HDM-sensitized PER than the common haplotype G-A (adjusted OR = 0.819, 95% CI = 0.676-0.993). The secondary structure of GARP altered in response to different genotypes of rs79525962 and rs3781699. Conclusion: SNP rs79525962 in the GARP gene marks a risk locus of HDM-sensitized PER in Chinese Hans.

Endostatin induces normalization of blood vessels in colorectal cancer and promotes infiltration of CD8+ T cells to improve anti-PD-L1 immunotherapy.

Introduction: The purpose of this study was to evaluate recombinant human endostatin (rHE)-induced normalization of the tumor vasculature in colorectal cancer (CRC) and to evaluate the therapeutic effects of combined treatment with rHE and a programmed death ligand-1 (PD-L1) inhibitor. Methods: A mouse subcutaneous tumorigenesis model was established to evaluate the antitumor effects of endostatin combined with a PD-L1 inhibitor on CRC. Intravoxel incoherent motion diffusion-weighted magnetic resonance imaging (IVIM-DW MRI) was used to evaluate changes in the intratumor microcirculation in response to combined treatment with endostatin and a PD-L1 inhibitor. The infiltration density and function of CD8+ T cells in tumors were evaluated using flow cytometry. Finally, clinical specimens were used to evaluate the expression area of tumor vascular pericytes and CD8+ T cells in tumor tissues. Results: The antitumor effects of endostatin combined with a PD-L1 inhibitor were significantly greater than those of endostatin or a PD-L1 inhibitor alone. On the ninth day of intervention, the endostatin group showed significantly higher pseudo diffusion parameter (D*) and microvascular volume fraction (F) values in tumors than those in the control group or PD-L1 group. After 27 days of intervention, the endostatin groups showed significantly lower levels of vascular endothelial growth factor (VEGF) and transforming growth factor (TGF)-ß than those in the control group. Treatment of CD8+ T cells with endostatin for 24 h did not alter the expression levels of markers of reduced T-cell activity. However, endostatin reversed the VEGF-mediated inhibition of the secretion of interferon (IFN)-γ from T cells. The results in CRC clinical samples showed that treatment with endostatin induced significantly higher infiltration of CD8+ T cells compared with treatment that did not include endostatin. Furthermore, the expression area of pericytes was significantly positively related to the infiltration density of CD8+ T cells and overall survival time. Conclusion: Endostatin improved the antitumor effects of PD-L1 inhibitors on CRC, significantly increased the activity of CD8+ T cells, and synergistically improved the tumor treatment effect of the two inhibitors.

The m6A-methylated mRNA pattern and the activation of the Wnt signaling pathway under the hyper-m6A-modifying condition in the keloid.

Purpose: The present study was carried out to investigate the global m6A-modified RNA pattern and possible mechanisms underlying the pathogenesis of keloid. Method: In total, 14 normal skin and 14 keloid tissue samples were first collected on clinics. Then, three samples from each group were randomly selected to be verified with the Western blotting to determine the level of methyltransferase and demethylase. The total RNA of all samples in each group was isolated and subjected to the analysis of MeRIP sequencing and RNA sequencing. Using software of MeTDiff and htseq-count, the m6A peaks and differentially expressed genes (DEGs) were determined within the fold change >2 and p-value < 0.05. The top 10 pathways of m6A-modified genes in each group and the differentially expressed genes were enriched by the Kyoto Encyclopedia of Genes and Genomes signaling pathways. Finally, the closely associated pathway was determined using the Western blotting and immunofluorescence staining. Results: There was a higher protein level of WTAP and Mettl3 in the keloid than in the normal tissue. In the keloid samples, 21,020 unique m6A peaks with 6,573 unique m6A-associated genetic transcripts appeared. In the normal tissue, 4,028 unique m6A peaks with 779 m6A-associated modified genes appeared. In the RNA sequencing, there were 847 genes significantly changed between these groups, transcriptionally. The genes with m6A-methylated modification and the upregulated differentially expressed genes between two tissues were both mainly related to the Wnt signaling pathway. Moreover, the hyper-m6A-modified Wnt/ß-catenin pathway in keloid was verified with Western blotting. From the immunofluorescence staining results, we found that the accumulated fibroblasts were under a hyper-m6A condition in the keloid, and the Wnt/ß-Catenin signaling pathway was mainly activated in the fibroblasts. Conclusion: The fibroblasts in the keloid were under a cellular hyper-m6A-methylated condition, and the hyper-m6A-modified highly expressed Wnt/ß-catenin pathway in the dermal fibroblasts might promote the pathogenesis of keloid.

Intelligent cataract surgery supervision and evaluation via deep learning.

PURPOSE: To assess the performance of a deep learning (DL) algorithm for evaluating and supervising cataract extraction using phacoemulsification with intraocular lens (IOL) implantation based on cataract surgery (CS) videos. MATERIALS AND METHODS: DeepSurgery was trained using 186 standard CS videos to recognize 12 CS steps and was validated in two datasets that contained 50 and 21 CS videos, respectively. A supervision test including 50 CS videos was used to assess the DeepSurgery guidance and alert function. In addition, a real-time test containing 54 CSs was used to compare the DeepSurgery grading performance to an expert panel and residents. RESULTS: DeepSurgery achieved stable performance for all 12 recognition steps, including the duration between two pairs of adjacent steps in internal validation with an ACC of 95.06% and external validations with ACCs of 88.77% and 88.34%. DeepSurgery also recognized the chronology of surgical steps and alerted surgeons to order of incorrect steps. Six main steps are automatically and simultaneously quantified during the evaluation process (centesimal system). In a real-time comparative test, the DeepSurgery step recognition performance was robust (ACC of 90.30%). In addition, DeepSurgery and an expert panel achieved comparable performance when assessing the surgical steps (kappa ranged from 0.58 to 0.77). CONCLUSIONS: DeepSurgery represents a potential approach to provide a real-time supervision and an objective surgical evaluation system for routine CS and to improve surgical outcomes.

Dynamic changes in immune gene co-expression networks predict development of type 1 diabetes.

Significant progress has been made in elucidating genetic risk factors influencing Type 1 diabetes (T1D); however, features other than genetic variants that initiate and/or accelerate islet autoimmunity that lead to the development of clinical T1D remain largely unknown. We hypothesized that genetic and environmental risk factors can both contribute to T1D through dynamic alterations of molecular interactions in physiologic networks. To test this hypothesis, we utilized longitudinal blood transcriptomic profiles in The Environmental Determinants of Diabetes in the Young (TEDDY) study to generate gene co-expression networks. In network modules that contain immune response genes associated with T1D, we observed highly dynamic differences in module connectivity in the 600 days (~ 2 years) preceding clinical diagnosis of T1D. Our results suggest that gene co-expression is highly plastic and that connectivity differences in T1D-associated immune system genes influence the timing and development of clinical disease.