IPOP: An Integrative Plant Multi-omics Platform for Cross-species Comparison and Evolutionary Study.

The advent of high-throughput sequencing technologies has led to the production of a significant amount of omics data in plants, which serves as valuable assets for conducting cross-species multi-omics comparative analysis. Nevertheless, the current dearth of comprehensive platforms providing evolutionary annotation information and multi-species multi-omics data impedes users from systematically and efficiently performing evolutionary and functional analysis on specific genes. In order to establish an advanced plant multi-omics platform that provides timely, accurate, and high-caliber omics information, we collected 7 distinct types of omics data from 6 monocots, 6 dicots, and 1 moss, and reanalyzed these data using standardized pipelines. Additionally, we furnished homology information, duplication events, and phylostratigraphic stages of 13 species to facilitate evolutionary examination. Furthermore, the integrative plant omics platform (IPOP) is bundled with a variety of online analysis tools that aid users in conducting evolutionary and functional analysis. Specifically, the Multi-omics Integration Analysis tool is available to consolidate information from diverse omics sources, while the Transcriptome-wide Association Analysis tool facilitates the linkage of functional analysis with phenotype. To illustrate the application of IPOP, we conducted a case study on the YTH domain gene family, wherein we observed shared functionalities within orthologous groups and discerned variations in evolutionary patterns across these groups. To summarize, the IPOP platform offers valuable evolutionary insights and multi-omics data to the plant sciences community, effectively addressing the need for cross-species comparison and evolutionary research platforms. All data and modules within IPOP are freely accessible for academic purposes (http://omicstudio.cloud:4012/ipod/).

Effects of sodium-glucose cotransporter 2 inhibitors on serum uric acid in patients with type 2 diabetes mellitus: A systematic review and network meta-analysis.

AIMS: The present study aims to determine the effects of sodium-glucose cotransporter 2 (SGLT-2) inhibitors on the serum uric acid (SUA) levels of patients with type 2 diabetes mellitus (T2DM) in Asia. METHODS: PubMed, CENTRAL, Embase and Cochrane Library databases were searched for randomized controlled trials of SGLT-2 inhibitors in patients with T2DM up to 15 July 2021, without language or date restrictions. RESULTS: In total, 19 high-quality studies (4218 participants) were included in the present network meta-analysis. All of the included SGLT-2 inhibitors (empagliflozin, dapagliflozin, canagliflozin, ipragliflozin, luseogliflozin and tofogliflozin) significantly decreased SUA levels compared with those of the control [total standard mean difference -0.965, 95% CI (-1.029, -0.901), p = .000, I2  = 98.7%] in patients with T2DM. Subgroup analysis and meta-regression showed that the combined analysis of different inhibitors might lead to heterogeneity of the results. Therefore, among the SGLT-2 inhibitors, the results of the subsequent network meta-analysis revealed that luseogliflozin and dapagliflozin ranked the highest in terms of lowering SUA levels among the SGLT-2 inhibitors. Moreover, the network meta-analysis declared that luseogliflozin (1 and 10 mg) and dapagliflozin (5 mg) led to a superior reduction in SUA in patients with T2DM. CONCLUSIONS: SGLT-2 inhibitors could significantly reduce SUA levels in patients with T2DM, particularly luseogliflozin (1 and 10 mg) and dapagliflozin (5 mg) possess the best effects. Therefore, SGLT-2 inhibitors look extremely promising as an antidiabetes treatment option in patients with T2DM with high SUA.

Lipid accumulation-induced hepatocyte senescence regulates the activation of hepatic stellate cells through the Nrf2-antioxidant response element pathway.

Non-alcoholic fatty liver disease (NAFLD) has become the most prevalent chronic liver disease globally. Elderly individuals are at a higher risk of developing NAFLD with severe clinical outcomes. Although NAFLD is closely related to liver aging, the role of hepatocyte senescence in the progression of NAFLD, especially in the development of fibrosis, is still unclear. The early stage of NAFLD is mainly characterized by lipid accumulation in hepatocytes, which could lead to severe oxidative stress, causing cellular senescence. In the present study, hepatocytes cultured in the presence of free fatty acids to induce lipid deposition were used as a hepatocyte senescence model in vitro. Senescent hepatocytes significantly increased the activation of co-cultured primary hepatic stellate cells (HSCs) and the expression of pro-fibrosis molecules. Moreover, the antioxidant regulator nuclear factor erythroid 2-related factor 2 (Nrf2) that was upregulated in senescent hepatocytes was found to be related to the activation of co-cultured HSCs. The Nrf2 agonist sulforaphane, which upregulated the transcriptional activity of the Nrf2-antioxidant response element (ARE) pathway, remarkably inhibited hepatocyte senescence and its activation effect on HSCs. However, the liver tissue obtained from non-alcoholic steatohepatitis (NASH) mice with Nrf2 knockdown showed decreased antioxidation and significant liver senescence and fibrosis. In conclusion, this study confirmed that lipid accumulation induces hepatocyte senescence, which leads to HSC activation and development of hepatic fibrosis. Increasing the activity of the Nrf2-ARE antioxidant pathway in senescent hepatocytes elicited the opposite effect, suggesting that targeting Nrf2 may prevent or delay the progression of aging-related liver fibrosis in NASH.

The effect of gestational diabetes mellitus on fetal right heart growth in late-term pregnancy: A prospective study.

BACKGROUND: Gestational diabetes mellitus (GDM) is a complication of pregnancy strongly associated with an increased risk of structural fetal abnormalities. As the fetal heart grows quickly during the late-term pregnancy period, it is important to understand fetal heart growth before birth. This study explored how GDM affects fetal heart growth by evaluating basic echocardiography indicators during late pregnancy. METHODS: This prospective, longitudinal study included 63 GDM patients (GDM group) and 67 healthy pregnant women (control group). All subjects underwent fetal echocardiography scans at gestational weeks 28-32, 32-36, and 36-40. Twelve echocardiographic indicators were assessed at each observation and analyzed by using a mixed model. RESULTS: The left atrial diameter (LA) and left ventricular end-diastolic diameter (LV) similarly increased from the first to the third observation. The right ventricular end-diastolic diameter (RV) was significantly different between the groups, and a group × time interaction was detected. The tricuspid annular peak systolic velocity (s') increased more rapidly in the GDM than the control group during the first to second observations, and the group × time interaction was significant. The increase in the tricuspid annular plane systolic excursion (TAPSE) of the GDM group was "slow-fast", while that of the control group was "fast-slow", during three observations. After adjusting covariates, the group difference and interaction effect of TAPSE and RV remained significant. CONCLUSIONS: The differences in fetal right heart indicators between the GDM and control groups suggest that GDM may affect the structure and functional growth of the fetal right heart during late-term pregnancy.

Secretory galectin-3 induced by glucocorticoid stress triggers stemness exhaustion of hepatic progenitor cells.

Adult progenitor cell populations typically exist in a quiescent state within a controlled niche environment. However, various stresses or forms of damage can disrupt this state, which often leads to dysfunction and aging. We built a glucocorticoid (GC)-induced liver damage model of mice, found that GC stress induced liver damage, leading to consequences for progenitor cells expansion. However, the mechanisms by which niche factors cause progenitor cells proliferation are largely unknown. We demonstrate that, within the liver progenitor cells niche, Galectin-3 (Gal-3) is responsible for driving a subset of progenitor cells to break quiescence. We show that GC stress causes aging of the niche, which induces the up-regulation of Gal-3. The increased Gal-3 population increasingly interacts with the progenitor cell marker CD133, which triggers focal adhesion kinase (FAK)/AMP-activated kinase (AMPK) signaling. This results in the loss of quiescence and leads to the eventual stemness exhaustion of progenitor cells. Conversely, blocking Gal-3 with the inhibitor TD139 prevents the loss of stemness and improves liver function. These experiments identify a stress-dependent change in progenitor cell niche that directly influence liver progenitor cell quiescence and function.

Lipid-injured hepatocytes release sOPN to improve macrophage migration via CD44 engagement and pFak-NFκB signaling.

BACKGROUND: The key characteristics in the pathogenesis of nonalcoholic steatohepatitis (NASH) are hepatic lipotoxicity, inflammatory cell infiltration (activated macrophages, in part), and varying degrees of fibrosis. The fatty acid palmitate (PA) can cause hepatocyte cellular dysfunction, but whether and how this process contributes to macrophage-associated inflammation is not well understood. This study aimed to explore whether lipid-injured hepatocytes result in the secretion of osteopontin (sOPN), and how sOPN induces macrophage migration to steatosis hepatocytes. METHODS: Human hepatocellular carcinoma HepG2 cells were incubated with PA to establish the lipotoxicity in hepatocytes model in vitro. The released sOPN was isolated, characterized, and applied to macrophage-like cells differentiated from the human monocytic cell line THP-1 cells. C57BL/6 mice were fed either chow or a diet high in fructose-fat-glucose (FFG) to induce NASH in vivo. Some NASH model mice were also given siSPP1 for two weeks to inhibit the expression of OPN. Related tissues were collected and analyzed by histology, immunofluorescence, ELISA, qRT-PCR, and western blotting. RESULTS: PA upregulated OPN expression and release in human hepatocytes, which drove the migration of macrophages. Incubation of HepG2 cells with palmitate increased mRNA expression and secretion of OPN in cell culture supernatants. Compared with the BSA and siSPP1 groups, treatment with the supernatant derived from PA-treated hepatocytes promoted macrophage migration and activation. The sOPN induction of macrophage migration occurred via CD44 engagement and activation of the pFak-NFκB signaling pathway. Likewise, administration of siSPP1 to NASH mice inhibited the expression and release of OPN, which was associated with decreased liver dysfunction, inflammatory cell infiltration, and even fibrosis. CONCLUSIONS: sOPN, which is released from lipid-injured hepatocytes, emerges as a cytokine driving the migration of macrophages, contributing to an inflammatory response in NASH.

Microbial Protein out of Thin Air: Fixation of Nitrogen Gas by an Autotrophic Hydrogen-Oxidizing Bacterial Enrichment.

For the production of edible microbial protein (MP), ammonia generated by the Haber-Bosch process or reclaimed ammonia from waste streams is typically considered as the nitrogen source. These processes for ammonia production are highly energy intensive. In this study, the potential for using nitrogen gas (N2) as a direct nitrogen source for MP production by hydrogen-oxidizing bacteria (HOB) was evaluated. The use of N2 versus ammonium as nitrogen source during the enrichment process resulted in differentiation of the bacterial community composition of the enrichments. A few previously unknown potential N2-fixing HOB taxa (i.e., representatives of the genus Azonexus and the family Comamonadaceae) dominated the enrichments. The biomass yield of a N2-fixing HOB enrichment was 30-50% lower than that of the ammonium-based HOB enrichment from the same inoculum source. The dried biomass of N2-fixing HOB had a high protein content (62.0 ± 6.3%) and an essential amino acid profile comparable to MP from ammonium-based HOB. MP from N2-fixing HOB could potentially be produced in situ without entailing the emissions caused by ammonia production and transportation by conventional means. It could be a promising substitute for N2-fixing protein-rich soybean because it has 70% higher protein content and double energy conversion efficiency from solar energy to biomass.

Thermal transport properties of novel two-dimensional CSe.

Recently, as a novel member of the IV-VI group compounds, two-dimensional (2D) buckled monolayer CSe has been discovered for use in high-performance light-emitting devices (Q. Zhang, Y. Feng, X. Chen, W. Zhang, L. Wu and Y. Wang, Nanomaterials, 2019, 9, 598). However, to date, the heat transport properties of this novel CSe is still lacking, which would hinder its potential application in electronic devices and thermoelectric materials that can generate electricity from waste heat. Here we systematically study the heat transport properties of monolayer CSe based on ab initio calculations and phonon Boltzmann transport theory. We find that the lattice thermal conductivity κlat of monolayer CSe is around 42 W m-1 K-1 at room temperature, which is much lower than those of black phosphorene, buckled phosphorene, MoS2, and buckled arsenene. Moreover, the longitudinal acoustic phonon mode contributes the most to the κlat, which is much larger than those of the out-of-plane phonon mode and transverse acoustic branches. The calculated size-dependent κlat shows that the sample size can significantly reduce the κlat of monolayer CSe and can persist up to 10 µm. These discoveries provide new insight into the size-dependent thermal transport in nanomaterials and guide the design of CSe-based low-dimensional quantum devices, such as thermoelectric devices.

Identification and study of differentially expressed miRNAs in aged NAFLD rats based on high-throughput sequencing.

INTRODUCTION AND OBJECTIVES: Hepatic microRNA (miR) expression profiles were explored in aged rats with NAFLD, in order to clarify the molecular mechanisms underlying the pathophysiological processes of aging-related NAFLD. PATIENTS OR MATERIALS AND METHODS: 24 aged rats (18-month-old) and 24 young rats (2-month-old) were randomly divided into two subgroups according to diet, control group and NAFLD group. After 8 weeks of administering 45% high-fat diet or normal diet, total hepatic RNA was extracted from liver tissues of the aged rats. Differentially expressed microRNAs (DE-miRs) in aged NAFLD group were detected and screened out using high-throughput sequencing technology. The data were subjected to Gene Ontology functional enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analyses using a bioinformatics approach. The sequencing results were further verified by RT-qPCR. RESULTS: Compared with the aged control liver tissues, 6 significantly upregulated miRs (miR-881-3p, miR-871-3p, miR-335, miR-223-3p, miR-155-5p, miR-146b-5p) and 4 significantly downregulated miRs (miR-182, miR-193-3p, miR-31a-5p and miR-96-5p) were identified in the aged NAFLD liver tissues. These DE-miRs were found to be involved in the regulation of cell signaling transduction and metabolism processes, probably affecting signaling pathways relevant to insulin secretion and some senile diseases. RT-qPCR results corroborated the sequencing results and demonstrated that 6 significantly upregulated miRs were not identified in the young group. CONCLUSIONS: A total of 10 DE-miRs identified in the aged NAFLD rats were involved in some certain insulin secretion and age-related functional pathways, which may serve as novel candidate targets for the diagnosis and treatment of aging-associated NAFLD.

Enriched hydrogen-oxidizing microbiomes show a high diversity of co-existing hydrogen-oxidizing bacteria.

While numerous reports exist on the axenic culturing of different hydrogen-oxidizing bacteria (HOB), knowledge about the enrichment of microbial communities growing on hydrogen, oxygen, and carbon dioxide as sole carbon and energy sources remains negligible. We want to elucidate if in such enrichments, most enriched populations are HOBs or heterotrophic organisms. In the present study, bacteria enriched from a soil sample and grown over 5 transfers using a continuous supply of hydrogen, oxygen, and carbon dioxide to obtain an enriched autotrophic hydrogen-oxidizing microbiome. The success of the enrichment was evaluated by monitoring ammonium consumption and biomass concentration for 120 days. The shift in the microbial composition of the original soil inoculum and all transfers was observed based on 16S rRNA amplicon sequencing. The hydrogen-oxidizing facultative chemolithoautotroph Hydrogenophaga electricum was isolated and found to be one of the abundant species in most transfers. Moreover, Achromobacter was isolated both under heterotrophic and autotrophic conditions, which was characterized as a hydrogen-oxidizing bacterium. The HOB enrichment condition constructed in this study provided an environment for HOB to develop and conquer in all transfers. In conclusion, we showed that enrichments on hydrogen, oxygen, and carbon dioxide as sole carbon and energy sources contain a diverse mixture of HOB and heterotrophs that resulted in a collection of culturable isolates. These isolates can be useful for further investigation for industrial applications.

Opposing Control by Transcription Factors MYB61 and MYB3 Increases Freezing Tolerance by Relieving C-Repeat Binding Factor Suppression.

Cold acclimation is an important process by which plants respond to low temperature and enhance their winter hardiness. C-REPEAT BINDING FACTOR1 (CBF1), CBF2, and CBF3 genes were shown previously to participate in cold acclimation in Medicago truncatula In addition, MtCBF4 is transcriptionally induced by salt, drought, and cold stresses. We show here that MtCBF4, shown previously to enhance drought and salt tolerance, also positively regulates cold acclimation and freezing tolerance. To identify molecular factors acting upstream and downstream of the MtCBF4 transcription factor (TF) in cold responses, we first identified genes that are differentially regulated upon MtCBF4 overexpression using RNAseq Digital Gene Expression Profiling. Among these, we showed that MtCBF4 directly activates the transcription of the COLD ACCLIMATION SPECIFIC15 (MtCAS15) gene. To gain insights into how MtCBF4 is transcriptionally regulated in response to cold, an R2R3-MYB TF, MtMYB3, was identified based on a yeast one-hybrid screen as binding directly to MYB cis-elements in the MtCBF4 promoter, leading to the inhibition of MtCBF4 expression. In addition, another MYB TF, MtMYB61, identified as an interactor of MtMYB3, can relieve the inhibitory effect of MtMYB3 on MtCBF4 transcription. This study, therefore, supports a model describing how MtCBF4 is regulated by antagonistic MtMYB3/MtMYB61 TFs, leading to the up-regulation of downstream targets such as MtCAS15 acting in cold acclimation in M. truncatula.

De novo transcriptome analysis of Medicago falcata reveals novel insights about the mechanisms underlying abiotic stress-responsive pathway.

BACKGROUND: The entire world is facing a deteriorating environment. Understanding the mechanisms underlying plant responses to external abiotic stresses is important for breeding stress-tolerant crops and herbages. Phytohormones play critical regulatory roles in plants in the response to external and internal cues to regulate growth and development. Medicago falcata is one of the stress-tolerant candidate leguminous species and is able to fix atmospheric nitrogen. This ability allows leguminous plants to grow in nitrogen deficient soils. METHODS: We performed Illumina sequencing of cDNA prepared from abiotic stress treated M. falcata. Sequencedreads were assembled to provide a transcriptome resource. Transcripts were annotated using BLASTsearches against the NCBI non-redundant database and gene ontology definitions were assigned. Acomparison among the three abiotic stress treated samples was carried out. The expression of transcriptswas confirmed with qRT-PCR. RESULTS: We present an abiotic stress-responsive M. falcata transcriptome using next-generation sequencing data from samples grown under standard, dehydration, high salinity, and cold conditions. We combined reads from all samples and de novo assembled 98,515 transcripts to build the M. falcata gene index. A comprehensive analysis of the transcriptome revealed abiotic stress-responsive mechanisms underlying the metabolism and core signalling components of major phytohormones. We identified nod factor signalling pathways during early symbiotic nodulation that are modified by abiotic stresses. Additionally, a global comparison of homology between the M. falcata and M. truncatula transcriptomes, along with five other leguminous species, revealed a high level of global sequence conservation within the family. CONCLUSIONS: M. falcata is shown to be a model candidate for studying abiotic stress-responsive mechanisms in legumes. This global gene expression analysis provides new insights into the biochemical and molecular mechanisms involved in the acclimation to abiotic stresses. Our data provides many gene candidates that might be used for herbage and crop breeding. Additionally, FalcataBase ( http://bioinformatics.cau.edu.cn/falcata/ ) was built for storing these data.

Aliskiren-attenuated myocardium apoptosis via regulation of autophagy and connexin-43 in aged spontaneously hypertensive rats.

There are controversies about the mechanism of myocardium apoptosis in hypertensive heart disease. The aim of this study was to investigate the relationship among autophagy, Cx43 and apoptosis in aged spontaneously hypertensive rats (SHRs) and establish whether Aliskiren is effective or not for the treatment of myocardium apoptosis. Twenty-one SHRs aged 52 weeks were randomly divided into three groups, the first two receiving Aliskiren at a dose of 10 and 25 mg/kg/day respectively; the third, placebo for comparison with seven Wistar-Kyoto (WKY) as controls. After a 2-month treatment, systolic blood pressure (SBP), heart to bw ratios (HW/BW%) and angiotensin II (AngII) concentration were significantly enhanced in SHRs respectively. Apoptotic cardiomyocytes detected with TUNEL and immunofluorescent labelling for active caspase-3 increased nearly fourfolds in SHRs, with a decline in the expression of survivin and AKT activation, and an increase in caspase-3 activation and the ratio of Bax/Bcl-2. Myocardium autophagy, detected with immunofluorescent labelling for LC3-II, increased nearly threefolds in SHRs, with the up-regulation of Atg5, Atg16L1, Beclin-1 and LC3-II. The expression of Cx43 plaque was found to be down-regulated in SHRs. Aliskiren significantly reduced SBP, HW/BW%, AngII concentration and the expression of AT(1)R. Thus, Aliskiren protects myocardium against apoptosis by decreasing autophagy, up-regulating Cx43. These effects showed a dose-dependent tendency, but no significance. In conclusion, the myocardium apoptosis developed during the hypertensive end-stage of SHRs could be ameliorated by Aliskiren via the regulation of myocardium autophagy and maladaptive remodelling of Cx43.

The neurovascular protective effects of huperzine A on D-galactose-induced inflammatory damage in the rat hippocampus.

BACKGROUND: Chronic administration of D-galactose (D-gal) results in oxidative stress and chronic inflammatory aging. Age-related changes in the brain result in neurovascular damage and blood-brain barrier (BBB) dysfunction. However, little is known regarding D-gal-induced neurovascular damage, as well as the protective effects of huperzine A. OBJECTIVE: The purpose of this study was to utilize a D-gal-induced rat model to investigate the activation of neurovascular inflammatory damage and apoptosis in the rat hippocampus and to understand whether huperzine A alleviates D-gal-induced neuronal and vascular inflammatory injury. METHODS: Aging rats were treated with D-gal (300 mg/kg s.c. for 8 weeks), were coadministered D-gal and huperzine A (D-gal 300 mg/kg and huperzine A 0.1 mg/kg s.c. for 8 weeks) or served as the saline-treated control group rats (same volume of saline given subcutaneously for 8 weeks). Changes in hippocampal morphology and biomarkers of inflammatory damage were analyzed. RESULTS: Our study revealed that chronic administration of D-gal resulted in the activation of glia and vascular endothelial cells and upregulation of mRNA and protein levels of cell-associated adhesion molecules and inflammatory cytokines via nuclear factor (NF)-κB inhibitor degradation and NF-κB nuclear translocation. The inflammatory injury caused significant BBB dysfunction, decreased density of tight junctions (TJs) and apoptosis in the rat hippocampus. Coadministration of huperzine A not only markedly inhibited the D-gal-induced increase in acetylcholinesterase (AChE) activity, but also alleviated D-gal-induced neurovascular damage by inhibiting D-gal-induced NF-κB activation, improving cerebrovascular function and suppressing the D-gal-induced decrease in the density and protein levels of TJs and cell apoptosis. CONCLUSIONS: Our findings provided evidence that D-gal induced a proinflammatory phenotype mediated by NF-κB in the rat hippocampus. Moreover, huperzine A suppressed D-gal-induced neurovascular damage and BBB dysfunction, partly by preventing NF-κB nuclear translocation. The inhibiting effect of huperzine A on AChE activity might play an important role in attenuating D-gal-induced inflammatory damage.

Inhibiting CB1 receptors improves lipogenesis in an in vitro non-alcoholic fatty liver disease model.

BACKGROUND: The endocannabinoids system (ECs) mediated mainly by CB1 and CB2 receptors plays an important role in non-alcoholic fatty liver disease by regulating lipid metabolism. This study is to further investigate the expression of CB1 and CB2 in the fat accumulation liver cells and to identify possible underlying mechanism by detecting the key lipogenesis factors. METHODS: Sodium oleate and sodium palmitate were added into the HepG2 cell line for forming fat accumulation liver cell. MTT assay was used to test the cell's cytotoxicity. The accumulation rate of fat in HepG2 cell was analyzed by the fluorescent staining. The mRNA and protein expression levels of CB1, CB2, SREBP-1c, ChREBP, L-PK, ACC1, FAS, LXRs and RXR were detected by RT-PCR and Western blot before and after the use of the antagonist. RESULTS: The receptors of CB1 were expressed in HepG2 cells with low levels while in HepG2 fatty liver cells with higher levels (p < 0.05). However, after the application of antagonist, the expressions were significantly decreased (p < 0.05). The expressions of SREBP-1c, ChREBP and LXRs were detectable in HepG2 cells and the expressions were increased in HepG2 fatty liver cells (p < 0.05). After using the antagonists, the expressions of SREBP-1c, ChREBP, LXRs, ACC1 and FAS were significantly decreased (p < 0.05). But L-PK and RXR changed little in two groups (p > 0.05). CONCLUSION: Results of the present study demonstrated that CB1 receptors had important pathophysiological effects on the formation of fatty liver. CB1 receptors could be regulated by SREBP-1c, ChREBP and LXRs. Therefore, targeting CB1 receptors for the treatment of NAFLD might have a potential application value.

Dual-Extraction Modeling: A multimodal deep learning architecture for phenotypic prediction and functional gene mining of complex traits.

Despite considerable advancements in extracting crucial insights from bio-omics data to unravel the intricate mechanisms underlying complex traits, the absence of a universal multimodal computational tool with robust interpretability for accurate phenotype prediction and identification of trait-associated genes remains a challenge. This study introduces the Dual-Extraction Modeling (DEM) approach, a multimodal deep learning architecture designed to extract representative features from heterogeneous omics datasets, enabling the prediction of complex trait phenotypes. Through comprehensive benchmarking experiments, we demonstrate DEM's efficacy in classification and regression prediction of complex traits. DEM consistently exhibits superior accuracy, robustness, generalizability, and flexibility. Notably, we establish its effectiveness in predicting pleiotropic genes influencing both flowering time and rosette leaf number, underscoring its commendable interpretability. Additionally, user-friendly software has been developed to facilitate the seamless utilization of DEM's functions. In summary, this study presents a state-of-the-art approach with the capability to effectively predict qualitative and quantitative traits, as well as identify functional genes, affirming its potential as a valuable tool in exploring the genetic basis of complex traits. Source code and software of DEM are available at https://github.com/cma2015/DEM/.

A novel electrolytic gas lift reactor for efficient microbial electrosynthesis of acetate from carbon dioxide.

The low current density impedes the practical application of microbial electrosynthesis for CO2 fixation. Engineering the reactor design is an effective way to increase the current density, especially for H2-mediated microbial electrosynthesis reactors. The electrolytic bubble column microbial electrosynthesis reactor has shown great potential for scaling up, but the mixing and gas mass transfer still need to be enhanced to further increase the current density. Here, we introduced an inner draft tube to the bubble column to tackle the problem. The addition of draft tube resulted in a 76.6% increase in the volumetric mass transfer coefficient (kLa) of H2, a 40% increase in the maximum current density (337 A/m2) and a 72% increase in average acetate production rate (3.1 g/L/d). The computational fluid dynamics simulations showed that the addition of draft tube enhanced mixing efficiency by enabling a more ordered cyclic flow pattern and a more uniform gas/liquid distribution. These results indicate that the electro-bubble column reactor with draft tube holds great potential for industrial implementation.

Elevated COX2 expression and PGE2 production by downregulation of RXRα in senescent macrophages.

Increased systemic level of inflammatory cytokines leads to numerous age-related diseases. In senescent macrophages, elevated prostaglandin E2 (PGE2) production contributes to the suppression of T cell function with aging, which increases the susceptibility to infections. However, the regulation of these inflammatory cytokines and PGE2 with aging still remains unclear. We have verified that cyclooxygenase (COX)-2 expression and PGE2 production are higher in LPS-stimulated macrophages from old mice than that from young mice. Downregulation of RXRα, a nuclear receptor that can suppress NF-κB activity, mediates the elevation of COX2 expression and PGE2 production in senescent macrophages. We also have found less induction of ABCA1 and ABCG1 by RXRα agonist in senescent macrophages, which partially accounts for high risk of atherosclerosis in aged population. Systemic treatment with RXRα antagonist HX531 in young mice increases COX2, TNF-α, and IL-6 expression in splenocytes. Our study not only has outlined a mechanism of elevated NF-κB activity and PGE2 production in senescent macrophages, but also provides RXRα as a potential therapeutic target for treating the age-related diseases.

Au core/Au-Ag alloy shell nanorods: composition- and shape-tailored optical responses.

A feasible way is developed to prepare Au core/Au-Ag alloy shell nanorods (Au@Au(x)Ag(1-x) NRs) based on co-reduction of gold and silver ions under the guidance of Au NRs templates. Alloy nanorods with a wide composition range (x tunable from 0 to 1) are obtained. The Ag+/Au3+ ratios are found to affect the detailed morphology of the endcaps, which is responsible for the abnormal red-shift of localized surface plasmon resonance (SPR) mode. In consensus with theoretical prediction, dielectric sensitivity of the alloy NRs is mainly determined by the maximum of the LSPR band. Due to the change in electron structure, the alloy shells exhibit lower SERS activities than pure Ag shell.

Enhancement of acetate production in hydrogen-mediated microbial electrosynthesis reactors by addition of silica nanoparticles.

Microbial electrosynthesis (MES) is a promising technology for CO2 fixation and electrical energy storage. Currently, the low current density of MES limits its practical application. The H2-mediated and non-biofilm-driven MES could work under higher current density, but it is difficult to achieve high coulombic efficiency (CE) due to low H2 solubility and poor mass transfer. Here, we proposed to enhance the hydrogen mass transfer by adding silica nanoparticles to the reactor. At pH 7, 35 â„ƒ and 39 A·m- 2 current density, with the addition of 0.3wt% silica nanoparticles, the volumetric mass transfer coefficient (kLa) of H2 in the reactor increased by 32.4% (from 0.37 h- 1 to 0.49 h- 1), thereby increasing the acetate production rate and CE of the reactor by 69.8% and 69.2%, respectively. The titer of acetate in the reactor with silica nanoparticles (18.5 g·L- 1) was 56.9% higher than that of the reactor without silica nanoparticles (11.8 g·L- 1). Moreover, the average acetate production rate of the reactor with silica nanoparticles was up to 2.14 g·L- 1·d- 1 in the stable increment phase, which was much higher than the other reported reactors. These results demonstrated that the addition of silica nanoparticles is an effective approach to enhancing the performance of H2-mediated MES reactors.