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Water scarcity is one of the major concerns of this century. The photocatalysis through TiO2 can be suitable for improving liquid wastewater treatment. However, TiO2 is used as a powder (nanoparticles), which is a drawback for full-scale applications. To overcome this, in the present work, powder TiO2 was impregnated on ceramic material. Several parameters, such as support cleanliness, support load, TiO2 suspension concentration, powder dispersion in a solvent, contact method, and drying temperature, were evaluated on the impregnation method. The influence of TiO2 concentration in suspensions was tested from 1 to 10% w/w. The results showed that the preparation conditions impact the TiO2 impregnation yield. The 10%TiO2/Leca was the most effective in photocatalysis but had a relevant loss of TiO2 from the support by erosion. For 3.6%TiO2/Leca and 5%TiO2/Leca, at TiO2 concentrations of 86.6 and 102.5 mg/L promoted 71 to 85% of sulfamethoxazole removal in 6 h under UVA radiation, respectively. Scanning electron microscopy (SEM) revealed the TiO2 adhesion onto the surface of the ceramic material, and the thickness of the TiO2 layer over the support can attain 7.64 to 10.9 μm. The work showed that the TiO2 impregnation method over Leca could be suitable for obtaining cost-effective photocatalysts.

Incineration bottom ashes (IBA) are the main waste from municipal solid waste (MSW) incineration. In the Iberian countries (Portugal and Spain), MSW incineration with energy recovery (WtE) plays an important role in MSW management. IBA is highly produced and managed differently both between and within countries. This paper aims to provide a comprehensive overview of the management model of IBA using the Iberian Peninsula as a case study, addressing its properties, current management, incentives and difficulties in valorizing, and prospects. For this purpose, incineration plants of both countries were approached, and a broad literature review was conducted to gather information. About 10% and 41% of IBA have been landfilled in Portugal and Spain, respectively. Metals (mostly ferrous) from Portuguese (6% of IBA) and Spanish (9% of IBA) WtE plants are recycled. In Portugal, the remaining IBA (84%) has been temporarily stored (11%), applied to landfills as a substitute for soil in intermediate and final covers, construction of paths, accesses, and platforms (41%), or used in civil engineering work and road construction (48%). In Spain, the remaining IBA (50%) has been reused mainly as a secondary raw material in the construction and civil engineering fields (77%), while the rest has been temporarily stored (11%), applied in the conditioning of landfills (4%), alsoa secondary aggregate replacing natural materials. Both countries regulate IBA reuse outside landfills but consider different requirements and criteria. Nevertheless, there are both drivers and barriers to valorization. In the future, different IBA applications will likely continue to be developed, with the concern of protecting the environment. Growing confidence in IBA reuse following the publication of proper studies is expected. Globally, uniform legal frameworks among EU members with the same standards would likely lead to better IBA valorization.

Water scarcity represents a problem for billions of people and is expected to get worse in the future. To guarantee people’s water needs, the use of “first-hand water” or the reuse of wastewater must be done. Wastewater treatment and reuse are favorable for this purpose, since first-hand water is scarce and the economic needs for the exploration of this type of water are increasing. In wastewater treatment, it is important to remove contaminants of emerging concern, as well as pathogenic agents. Parabens are used in daily products as preservatives and are detected in different water sources. These compounds are related to different human health problems due to their endocrine-disrupting behavior, as well as several problems in animals. Thus, their removal from water streams is essential to achieve safe reusable water. Advanced Oxidation Processes (AOPs) are considered very promising technologies for wastewater treatment and can be used as alternatives or as complements of the conventional wastewater treatments that are inefficient in the removal of such contaminants. Different AOP technologies such as ozonation, catalytic ozonation, photocatalytic ozonation, Fenton’s, and photocatalysis, among others, have already been used for parabens abatement. This manuscript critically overviews several AOP technologies used in parabens abatement. These treatments were evaluated in terms of ecotoxicological assessment since the resulting by-products of parabens abatement can be more toxic than the parent compounds. The economic aspect was also analyzed to evaluate and compare the considered technologies.

Parabens are widely used in different industries as preservatives and antimicrobial compounds. The evolution of analytical techniques allowed the detection of these compounds in different sources at µg/L and ng/L. Until today, parabens were already found in water sources, air, soil and even in human tissues. The impact of parabens in humans, animals and in ecosystems are a matter of discussion within the scientific community, but it is proven that parabens can act as endocrine disruptors, and some reports suggest that they are carcinogenic compounds. The presence of parabens in ecosystems is mainly related to wastewater discharges. This work gives an overview about the paraben problem, starting with their characteristics and applications. Moreover, the dangers related to their usage were addressed through the evaluation of toxicological studies over different species as well as of humans. Considering this, paraben detection in different water sources, wastewater treatment plants, humans and animals was analyzed based on literature results. A review of European legislation regarding parabens was also performed, presenting some considerations for the use of parabens.

The highly infiltrating nature of glioma cells is the major cause for the poor prognosis of brain malignancies. Motility, proliferation, and gene expression of cells in natural and synthetic gels have been analyzed by several authors, yet quantitative studies elucidating the role of matrix porosity and rigidity in the development of whole malignant masses are missing. Here, an experimental-computational framework is introduced to analyze the behavior of U87-MG cells and spheroids in compact hyaluronic acid gels (HA), replicating the brain parenchyma; and fibrous collagen gels (COL), resembling the organized structures of the brain. Experimentally it was observed that individual U87-MG cells in COL assumed an elongated morphology within a few hours post inclusion (p.i.) and travelled longer distances than in HA. As spheroids, U87-MG cells rapidly dispersed into COL resulting in infiltrating regions as large as tumor cores (≈600 μm, at 8 days p.i.). Conversely, cells in HA originated smaller and denser infiltrating regions (≈300 μm, at 8 days p.i.). Notably, COL tumor core size was only 20% larger than in HA, at longer time points. Computationally, by introducing for the first time the effects of matrix heterogeneity in our numerical simulations, the results confirmed that matrix porosity and its spatial organization are key factors in priming the infiltrating potential of these malignant cells. The experimental-numerical synergy can be used to predict the behavior of neoplastic masses under diverse conditions and the efficacy of combination therapies simultaneously aiming at killing cancer cells and modulating the tumor microenvironment.

Abstract Recruitment of non-canonical BCOR-PRC1.1 to non-methylated CpG islands via KDM2B plays a fundamental role in transcription control during developmental processes and cancer progression. However, the mechanism is still largely unknown on how this recruitment is regulated. Here, we unveiled the importance of the Poly-D/E regions within the linker of BCOR for its binding to KDM2B. Interestingly, we also demonstrated that these negatively charged Poly-D/E regions on BCOR play autoinhibitory roles in liquid-liquid phase separation (LLPS) of BCORANK-linker-PUFD/PCGF1RAWUL. Through neutralizing negative charges of these Poly-D/E regions, Ca2+ not only weakens the interaction between BCOR/PCGF1 and KDM2B, but also promotes co-condensation of the enzymatic core of BCOR-PRC1.1 with KDM2B into liquid-like droplet. Accordingly, we propose that Ca2+ could modulate the compartmentation and recruitment of the enzymatic core of BCOR-PRC1.1 on KDM2B target loci. Thus, our finding advances the mechanistic understanding on how the tethering of BCOR-PRC1.1 enzymatic core to KDM2B is regulated.

Recombinant human bone morphogenetic protein-2 (rhBMP-2) is the predominant growth factor that effectively induces osteogenic differentiation in orthopedic procedures. However, the bioactivity and stability of rhBMP-2 are intrinsically associated with its sequence, structure, and storage conditions. In this study, we successfully determined the amino acid sequence and protein secondary structure model of non-glycosylated rhBMP-2 expressed by an E. coli expression system through X-ray crystal structure analysis. Furthermore, we observed that acidic storage conditions enhanced the proliferative and osteoinductive activity of rhBMP-2. Although the osteogenic activity of non-glycosylated rhBMP-2 is relatively weaker compared to glycosylated rhBMP-2; however, this discrepancy can be mitigated by incorporating exogenous chaperone molecules. Overall, such information is crucial for rationalizing the design of stabilization methods and enhancing the bioactivity of rhBMP-2, which may also be applicable to other growth factors.

Abstract Cytokines have attracted sustained attention due to their multi-functional cellular response in immunotherapy. However, their application was limited to their short half-time, narrow therapeutic window, and undesired side effects. To address this issue, we developed a portable smart blue-light controlled (PSLC) device based on optogenetic technology. By combining this PSLC device with blue-light controlled gene modules, we successfully achieved the targeted regulation of cytokine expression within the tumor microenvironment. To alter the tumor microenvironment of solid tumors, pro-inflammatory cytokines were selected as blue-light controlled molecules. The results show that blue-light effectively regulates the expression of pro-inflammatory cytokines both in vitro and in vivo. This strategy leads to enhanced and activated tumor-infiltrating immune cells, which facilitated to overcome the immunosuppressive microenvironment, resulting in significant tumor shrinkage in tumor-bearing mice. Hence, our study offers a unique strategy for cytokine therapy and a convenient device for animal studies in optogenetic immunotherapy.

Summary: Calcitonin gene-related peptide (CGRP), a neuropeptide involved in nociceptor neuronal function, plays a critical role in mediating neuroinflammation and pain. In this study, we find that bladder group 2 innate lymphoid cells (ILC2s) function as primary producers of CGRP in the early phase of bacterial cystitis, contributing to increased inflammation, altered voiding behavior, and heightened pelvic allodynia. Furthermore, we demonstrate that interleukin (IL)-33, a cytokine secreted by urothelial cells, upregulates CGRP production by ILC2s in the bladder during uropathogenic Escherichia coli (UPEC) infection. Moreover, our research reveals that monocytes expressing high levels of receptor activity-modifying protein 1 (RAMP1), a CGRP receptor, mediate the pro-inflammatory effects of CGRP-producing ILC2s. In summary, our results underscore the significance of the immune cell-derived neuropeptides in the pathology of UPEC infection, suggesting a promising therapeutic approach targeting the IL-33-ILC2-CGRP axis for managing lower urinary tract symptoms in bacterial cystitis.

Abstract Accurate and sensitive near‐infrared (NIR) luminescent lateral flow immunoassay (LFIA) has attracted considerable attention in the field of point‐of‐care testing (POCT). However, the detection accuracy and sensitivity are often compromised by the low fluorescence quantum efficiency ( 800 nm) completely eliminated background interference and allowed highly accurate and sensitive detection without any pre‐treatment steps. The limits of detection (LODs) for aflatoxin B1 (AFB1) in soy sauce, alpha hemolysin (Hla) of Staphylococcus aureus biomarker in joint fluid, and C‐reactive protein (CRP) in human haemolysed samples were 0.01 ng mL−1, 0.02 µg mL−1, and 0.156 mg L−1, respectively, commensurating with those of the corresponding gold standard assays and covering the detection range of interests. It is anticipated that the ultrabright NIR AIEgen nanoparticles will serve as a universally applicable signal probe for NIR‐LFIA diagnostics, promising to expand the range of applications for quantitative detection of complex samples.

Introduction: Motoric cognitive risk syndrome (MCR), characterized by subjective cognitive complaints and slow gait in older populations, is associated with sleep duration. However, the association between MCR and daytime nap duration has not been thoroughly explored. Methods: Baseline data from the China Health and Retirement Longitudinal Study (CHARLS) were used in this study. MCR was defined as the coexistence of subjective cognitive complaints and objective slow gait speed without a history of dementia or mobility disability. Daytime nap duration was categorized into four groups: no napping, short napping (

Abstract From childhood to adolescence, the spatiotemporal development pattern of the human brain white matter connectome and its underlying transcriptomic and cellular mechanisms remain largely unknown. With a longitudinal diffusion MRI cohort of 604 participants, we map the developmental trajectory of the white matter connectome from global to regional levels and identify that most brain network properties followed a linear developmental trajectory. Importantly, connectome-transcriptomic analysis reveals that the spatial development pattern of white matter connectome is potentially regulated by the transcriptomic architecture, with positively correlated genes involve in ion transport- and development-related pathways expressed in excitatory and inhibitory neurons, and negatively correlated genes enriches in synapse- and development-related pathways expressed in astrocytes, inhibitory neurons and microglia. Additionally, the macroscale developmental pattern is also associated with myelin content and thicknesses of specific laminas. These findings offer insights into the underlying genetics and neural mechanisms of macroscale white matter connectome development from childhood to adolescence.

Huangjiu is known for its unique aroma, primarily attributed to its high concentration of β-phenylethanol (ranging from 40 to 130 mg/L). Phenylalanine aminotransferase Aro9p and phenylpyruvate decarboxylase Aro10p are key enzymes in the β-phenylethanol synthetic pathway of Saccharomyces cerevisiae HJ. This study examined the enzymatic properties of these two enzymes derived from S. cerevisiae HJ and S288C. After substrate docking, Aro9pHJ (−24.05 kJ/mol) and Aro10pHJ (−14.33 kJ/mol) exhibited lower binding free energies compared to Aro9pS288C (−21.93 kJ/mol) and Aro10pS288C (−12.84 kJ/mol). ARO9 and ARO10 genes were heterologously expressed in E. coli BL21. Aro9p, which was purified via affinity chromatography, showed inhibition by l-phenylalanine (L-PHE), but the reaction rate Vmax(Aro9pHJ: 23.89 μmol·(min∙g)−1) > Aro9pS288C: 21.3 μmol·(min∙g)−1) and inhibition constant Ki values (Aro9pHJ: 0.28 mol L−1>Aro9pS288C 0.26 mol L−1) indicated that Aro9p from S. cerevisiae HJ was more tolerant to substrate stress during Huangjiu fermentation. In the presence of the same substrate phenylpyruvate (PPY), Aro10pHJ exhibited a stronger affinity than Aro10pS288C. Furthermore, Aro9pHJ and Aro10pHJ were slightly more tolerant to the final metabolites β-phenylethanol and ethanol, respectively, compared to those from S288C. The study suggests that the mutations in Aro9pHJ and Aro10pHJ may contribute to the increased β-phenylethanol concentration in Huangjiu. This is the first study investigating enzyme tolerance mechanisms in terms of substrate and product, providing a theoretical basis for the regulation of the β-phenylethanol metabolic pathway.

Eschar and slough in wounds serve as a reservoir for microorganisms and biofilms, damaged/devitalised cells, and inflammatory chemokines/cytokines, which work to initiate and prolong persistent inflammation and increase the risk of infection. Biofilm-related inflammation and infections are considered to be highly prevalent in acute wounds and chronic wounds. As slough is known to harbour biofilms, measuring the efficacy of antimicrobials in killing microbes both within and under slough is warranted. This highlights the need for more clinically relevant wound biofilm models to address this significant clinical need. Consequently, in this study, we developed an in vitro artificial wound slough (AWS) biofilm model produced by forming a biofilm below a layer of AWS, the latter of which was composed of the main protein components reported in wound eschar and slough, namely collagen, elastin, and fibrin. The model was employed to investigate the antibiofilm and antibacterial efficacy of a new patented smart next-generation antibiofilm technology composed of silver–zinc EDTA complexes and designed as a family of multifunctional metal complexes referred to as MMCs, in a liquid format, and to determine both the performance and penetration through AWS to control and manage biofilms. The results demonstrated the ability of the AWS–biofilm model to be employed for the evaluation of the efficacy of a new antibiofilm and antimicrobial next-generation smart technology. The results also demonstrated the potential for the proprietary EDTA multifunctional metal complexes to be used for the disruption of biofilms, such as those that form in chronic wounds.

To address the limitations of traditional footstep vibration signal localization algorithms, such as limited accuracy, single feature extraction, and cumbersome parameter adjustment, a motion target localization method for step vibration signals based on deep learning is proposed. Velocity vectors are used to describe human motion and adapt it to the nonlinear motion and complex interactions of moving targets. In the feature extraction stage, a one-dimensional residual convolutional neural network is constructed to extract the time–frequency domain features of the signals, and a channel attention mechanism is introduced to enhance the model’s focus on different vibration sensor signal features. Furthermore, a bidirectional long short-term memory network is built to learn the temporal relationships between the extracted signal features of the convolution operation. Finally, regression operations are performed through fully connected layers to estimate the position and velocity vectors of the moving target. The dataset consists of footstep vibration signal data from six experimental subjects walking on four different paths and the actual motion trajectories of the moving targets obtained using a visual tracking system. Experimental results show that compared to WT-TDOA and SAE-BPNN, the positioning accuracy of our method has been improved by 37.9% and 24.8%, respectively, with a system average positioning error reduced to 0.376 m.

Bone defects caused by trauma, tumor resection, or developmental abnormalities are important issues in clinical practice. The vigorous development of tissue engineering technology provides new ideas and directions for regenerating bone defects. Hydroxyapatite (HAp), a bioactive ceramic, is extensively used in bone tissue engineering because of its excellent osteoinductive performance. However, its application is challenged by its single function and conventional environment-unfriendly synthesis methods. In this study, we successfully ''green'' synthesized sr-silk fibroin co-assembly hydroxyapatite nanoparticles (Sr-SF-HA) using silk fibroin (SF) as a biomineralized template, thus enabling it to have angiogenic activity and achieving the combination of organic and inorganic substances. Then, the rough composite microspheres loaded with Sr-SF-HA (CS/Sr-SF-HA) through electrostatic spraying technology and freeze-drying method were prepared. The CCK-8 test and live/dead cell staining showed excellent biocompatibility of CS/Sr-SF-HA. Alkaline phosphatase (ALP) staining, alizarin red staining (ARS), immunofluorescence, western blotting, and qRT-PCR test showed that CS/Sr-SF-HA activated the expression of related genes and proteins, thus inducing the osteogenic differentiation of rBMSCs. Moreover, tube formation experiments, scratch experiments, immunofluorescence, and qRT-PCR detection indicated that CS/Sr-SF-HA have good angiogenic activity. Furthermore, in vivo studies showed that the CS/Sr-SF-HA possesses excellent biocompatibility, vascular activity, as well as ectopic osteogenic ability in the subcutaneous pocket of rats. This study indicates that the construction of CS/Sr-SF-HA with angiogenic and osteogenic properties has great potential for bone tissue engineering.

Summary: During asymmetric division of Drosophila larval neuroblasts, the fate determinant Prospero (Pros) and its adaptor Miranda (Mira) are segregated to the basal cortex through atypical protein kinase C (aPKC) phosphorylation of Mira and displacement from the apical cortex, but Mira localization after aPKC phosphorylation is not well understood. We identify Kin17, a DNA replication and repair protein, as a regulator of Mira localization during asymmetric cell division. Loss of Kin17 leads to aberrant localization of Mira and Pros to the centrosome, cytoplasm, and nucleus. We provide evidence to show that the mislocalization of Mira and Pros is likely due to reduced expression of Falafel (Flfl), a component of protein phosphatase 4 (PP4), and defects in dephosphorylation of serine-96 of Mira. Our work reveals that Mira is likely dephosphorylated by PP4 at the centrosome to ensure proper basal localization of Mira after aPKC phosphorylation and that Kin17 regulates PP4 activity by regulating Flfl expression.

Summary: Stephania japonica is an early-diverging eudicotyledon plant with high levels of cepharanthine, proven to be effective in curing coronavirus infections. Here, we report a high-quality S. japonica genome. The genome size is 688.52 Mb, and 97.37% sequences anchor to 11 chromosomes. The genome comprises 67.46% repetitive sequences and 21,036 genes. It is closely related to two Ranunculaceae species, which diverged from their common ancestor 55.90–71.02 million years ago (Mya) with a whole-genome duplication 85.59–96.75 Mya. We further reconstruct ancestral karyotype of Ranunculales. Several cepharanthine biosynthesis genes are identified and verified by western blot. Two genes (Sja03G0243 and Sja03G0241) exhibit catalytic activity as shown by liquid chromatography-mass spectrometry. Then, cepharanthine biosynthesis genes, transcription factors, and CYP450 family genes are used to construct a comprehensive network. Finally, we construct an early-diverging eudicotyledonous genome resources (EEGR) database. As the first genome of the Menispermaceae family to be released, this study provides rich resources for genomic studies.

Abstract Background Systematic characterization of how genetic variation modulates gene regulation in a cell type-specific context is essential for understanding complex traits. To address this question, we profile gene expression and chromatin accessibility in cells from healthy retinae of 20 human donors through single-cell multiomics and genomic sequencing. Results We map eQTL, caQTL, allelic-specific expression, and allelic-specific chromatin accessibility in major retinal cell types. By integrating these results, we identify and characterize regulatory elements and genetic variants effective on gene regulation in individual cell types. The majority of identified sc-eQTLs and sc-caQTLs display cell type-specific effects, while the cis-elements containing genetic variants with cell type-specific effects are often accessible in multiple cell types. Furthermore, the transcription factors whose binding sites are perturbed by genetic variants tend to have higher expression levels in the cell types where the variants exert their effects, compared to the cell types where the variants have no impact. We further validate our findings with high-throughput reporter assays. Lastly, we identify the enriched cell types, candidate causal variants and genes, and cell type-specific regulatory mechanism underlying GWAS loci. Conclusions Overall, genetic effects on gene regulation are highly context dependent. Our results suggest that cell type-dependent genetic effect is driven by precise modulation of both trans-factor expression and chromatin accessibility of cis-elements. Our findings indicate hierarchical collaboration among transcription factors plays a crucial role in mediating cell type-specific effects of genetic variants on gene regulation.

Abstract Background Pancreatic cancer stem cells (CSCs) promote pancreatic ductal adenocarcinoma (PDAC) tumorigenesis and chemoresistance. Cyclin-dependent kinase 1 (CDK1) plays an important role in tumor initiation in other tumors, but the function of CDK1 in PDAC remains unclear. Fisetin is a bioactive flavonoid with anti-tumor properties in multiple tumors, while its function in CSCs remains elusive. Results In this study, we demonstrated that CDK1 was correlated with prognosis and was highly expressed in pancreatic cancer tissue and gemcitabine-resistant cells. Silencing CDK1 impaired tumor stemness and reduced a subset of CSCs. We found that fisetin blocked the kinase pocket domain of CDK1 and inhibited pancreatic CSC characteristics. Using acetylation proteomics analysis and phosphorylation array assay, we confirmed that fisetin reduced CDK1 expression and increased CDK1 acetylation at lysine 33 (K33), which resulted in the suppression of CDK1 phosphorylation. Silencing CDK1 or STAT3 suppressed tumor stemness properties, while overexpressing CDK1 or STAT3 showed the opposite effect. Mutation or acetylation of CDK1 at K33 weakened STAT3 phosphorylation at Y705, impairing the expression of stem-related genes and pancreatic cancer stemness. In addition, lack of histone deacetylase 3 (HDAC3), which deacetylates CDK1, contributed to weakening STAT3 phosphorylation by regulating the post-translational modification of CDK1, thereby decreasing the stemness of PDAC. Moreover, our results revealed that fisetin enhanced the effect of gemcitabine through eliminating a subpopulation of pancreatic CSCs by inhibiting the CDK1–STAT3 axis in vitro and in vivo. Conclusion Our findings highlight the role of post-translational modifications of CDK1–STAT3 signaling in maintaining cancer stemness of PDAC, and indicated that targeting the CDK1–STAT3 axis with inhibitors such as fisetin is a potential therapeutic strategy to diminish drug resistance and eliminate PDAC.

Autophagy plays a vital role in cell homeostasis by eliminating nonfunctional components and promoting cell survival. Here, we examined the levels of autophagy signaling proteins after 7 days of overload hypertrophy in the extensor digitorum longus (EDL) and soleus muscles of control and diabetic rats. We compared control and 3‐day streptozotocin‐induced diabetic rats, an experimental model for type 1 diabetes mellitus (T1DM). EDL muscles showed increased levels of basal autophagy signaling proteins. The diabetic state did not affect the extent of overload‐induced hypertrophy or the levels of autophagy signaling proteins (p‐ULK1, Beclin‐1, Atg5, Atg12‐5, Atg7, Atg3, LC3‐I and II, and p62) in either muscle. The p‐ULK‐1, Beclin‐1, and p62 protein expression levels were higher in the EDL muscle than in the soleus before the hypertrophic stimulus. On the contrary, the soleus muscle exhibited increased autophagic signaling after overload‐induced hypertrophy, with increases in Beclin‐1, Atg5, Atg12‐5, Atg7, Atg3, and LC3‐I expression in the control and diabetic groups, in addition to p‐ULK‐1 in the control groups. After hypertrophy, Beclin‐1 and Atg5 levels increased in the EDL muscle of both groups, while p‐ULK1 and LC3‐I increased in the control group. In conclusion, the baseline EDL muscle exhibited higher autophagy than the soleus muscle. Although TDM1 promotes skeletal muscle mass loss and strength reduction, it did not significantly alter the extent of overload‐induced hypertrophy and autophagy signaling proteins in EDL and soleus muscles, with the two groups exhibiting different patterns of autophagy activation.

Detecting anomalies in texture has become a significant concern across various industrial processes. One prevalent application of this is in inspecting patterned textures, especially in the domain of fabric defect detection, which is a commonly encountered scenario. This task entails dealing with a wide array of colours and textile varieties, spanning a broad spectrum of fabrics. Due to the extensive diversity in colours, textures, and defect characteristics, fabric defect detection presents a complex and formidable challenge within the realm of patterned texture inspection. While recent trends have seen a rise in the utilization of deep learning methods for anomaly detection, there still exist notable gaps in this field. In this paper, we introduce a novel dataset comprising a diverse selection of fabrics and defects from a textile company based in Portugal. Our contributions encompass the provision of this unique dataset and the evaluation of state-of-the-art (SOTA) methods’ performance on our dataset.

The Gorongosa National Park (Mozambique) is one of the most emblematic protected areas in Africa, well known for its vertebrate biodiversity and restoration ecology efforts following the Mozambican civil war in 1992. The invertebrate biodiversity of Gorongosa National Park is still poorly studied, although the scarce information available indicates the existence of a rich number of species, namely in the case of tiger- and ground-beetles (Coleoptera, Caraboidea). Moreover, the study of arthropod assemblages is key for designing conservation practices since they are potentially accurate biodiversity and ecological indicators. Hence, the diversity assessment of Caraboidea beetles using standardised methodologies is likely to provide a new insight for future conservation planning and help to quantify the effects of climate change in areas identified as vulnerable to anthropogenic pressures, such as the Gorongosa National Park.We report the occurrence of five tiger beetles (Cicindelidae) and 93 ground-beetles (Carabidae) species/morphospecies in Gorongosa National Park from a field survey funded by the ECOASSESS project. Sampling was performed in the four main habitat types present in the Park (miombo tropical forest, mixed dry forest, transitional forest and grasslands) between 25 October and 25 November 2019. In this sampling window, the turnover of Caraboidea species from the dry season to the wet season was recorded for the first time. Twenty-eight species of ground-beetles are new records to Mozambique, including three new subgenera and three new genera. Additional information on species phenology and habitat preferences is also provided.

Abstract The two most prevalent subtypes of epithelial ovarian carcinoma (EOC) are ovarian clear cell carcinoma (OCCC) and high-grade serous ovarian carcinoma (HGSC). Patients with OCCC have a poor prognosis than those with HGSC due to chemoresistance, implying the need for novel treatment target. In this study, we applied single-cell RNA sequencing (scRNA-seq) together with bulk RNA-seq data from the GEO (Gene Expression Omnibus) database (the GSE189553 dataset) to characterize and compare tumor heterogeneity and cell-level evolution between OCCC and HGSC samples. To begin, we found that the smaller proportion of an epithelial OCCC cell subset in the G2/M phase might explain OCCC chemoresistance. Second, we identified a possible pathogenic OCCC epithelial cell subcluster that overexpresses LEFTY1. Third, novel biomarkers separating OCCC from HGSC were discovered and subsequently validated on a wide scale using immunohistochemistry. Amine oxidase copper containing 1 (AOC1) was preferentially expressed in OCCC over HGSC, while S100 calcium-binding protein A2 (S100A2) was detected less frequently in OCCC than in HGSC. In addition, we discovered that metabolic pathways were enriched in the epithelial compartment of the OCCC samples. In vitro experiments verified that inhibition of oxidative phosphorylation or glycolysis pathways exerted direct antitumor effects on both OCCC and HGSC cells, while targeting glutamine metabolism or ferroptosis greatly attenuated chemosensitivity only in OCCC cells. Finally, to determine whether there were any variations in immune cell subsets between OCCC and HGSC, data from scRNA-seq and mass cytometry were pooled for analysis. In summary, our work provides the first holistic insights into the cellular and molecular distinctions between OCCC and HGSC and is a valuable source for discovering new targets to leverage in clinical treatments to improve the poor prognosis of patients with OCCC.

Abstract Despite decades of genetic studies on late-onset Alzheimer’s disease, the underlying molecular mechanisms remain unclear. To better comprehend its complex etiology, we use an integrative approach to build robust predictive (causal) network models using two large human multi-omics datasets. We delineate bulk-tissue gene expression into single cell-type gene expression and integrate clinical and pathologic traits, single nucleotide variation, and deconvoluted gene expression for the construction of cell type-specific predictive network models. Here, we focus on neuron-specific network models and prioritize 19 predicted key drivers modulating Alzheimer’s pathology, which we then validate by knockdown in human induced pluripotent stem cell-derived neurons. We find that neuronal knockdown of 10 of the 19 targets significantly modulates levels of amyloid-beta and/or phosphorylated tau peptides, most notably JMJD6. We also confirm our network structure by RNA sequencing in the neurons following knockdown of each of the 10 targets, which additionally predicts that they are upstream regulators of REST and VGF. Our work thus identifies robust neuronal key drivers of the Alzheimer’s-associated network state which may represent therapeutic targets with relevance to both amyloid and tau pathology in Alzheimer’s disease.

Abstract Background Colorectal cancer (CRC) is one of the most common cancers in the world. Oxidative stress reactions have been reportedly associated with oncogenesis and tumor progression. By analyzing mRNA expression data and clinical information from The Cancer Genome Atlas (TCGA), we aimed to construct an oxidative stress-related long noncoding RNA (lncRNA) risk model and identify oxidative stress-related biomarkers to improve the prognosis and treatment of CRC. Results Differentially expressed oxidative stress-related genes (DEOSGs) and oxidative stress-related lncRNAs were identified by using bioinformatics tools. An oxidative stress-related lncRNA risk model was constructed based on 9 lncRNAs (AC034213.1, AC008124.1, LINC01836, USP30-AS1, AP003555.1, AC083906.3, AC008494.3, AC009549.1, and AP006621.3) by least absolute shrinkage and selection operator (LASSO) analysis. The patients were then divided into high- and low-risk groups based on the median risk score. The high-risk group had a significantly worse overall survival (OS) (p

Automatically segmenting polyps from colonoscopy videos is crucial for developing computer-assisted diagnostic systems for colorectal cancer. Existing automatic polyp segmentation methods often struggle to fulfill the real-time demands of clinical applications due to their substantial parameter count and computational load, especially those based on Transformer architectures. To tackle these challenges, a novel lightweight long-range context fusion network, named LightCF-Net, is proposed in this paper. This network attempts to model long-range spatial dependencies while maintaining real-time performance, to better distinguish polyps from background noise and thus improve segmentation accuracy. A novel Fusion Attention Encoder (FAEncoder) is designed in the proposed network, which integrates Large Kernel Attention (LKA) and channel attention mechanisms to extract deep representational features of polyps and unearth long-range dependencies. Furthermore, a newly designed Visual Attention Mamba module (VAM) is added to the skip connections, modeling long-range context dependencies in the encoder-extracted features and reducing background noise interference through the attention mechanism. Finally, a Pyramid Split Attention module (PSA) is used in the bottleneck layer to extract richer multi-scale contextual features. The proposed method was thoroughly evaluated on four renowned polyp segmentation datasets: Kvasir-SEG, CVC-ClinicDB, BKAI-IGH, and ETIS. Experimental findings demonstrate that the proposed method delivers higher segmentation accuracy in less time, consistently outperforming the most advanced lightweight polyp segmentation networks.

The sclerotium of the edible mushroom Polyporus umbellatus (Zhuling) exhibits various medicinal properties. However, given its long growth cycle and overexploitation, wild resources are facing depletion. Macrofungal growth depends on diverse microbial communities; however, the impact of soil bacteria on P. umbellatus development is unknown. Here, we combined high-throughput sequencing and pure culturing to characterize the diversity and potential function of bacteria and fungi inhabiting the P. umbellatus sclerotium and tested the bioactivities of their isolates. Fungal operational taxonomic units (OTUs) were clustered and classified, revealing 1275 genera. Bacterial OTUs yielded 891 genera. Additionally, 81 bacterial and 15 fungal strains were isolated from P. umbellatus sclerotia. Antagonism assays revealed three bacterial strains (FN2, FL19, and CL15) promoting mycelial growth by producing indole-3-acetic acid, solubilizing phosphate, and producing siderophores, suggesting their role in regulating growth, development, and production of active compounds in P. umbellatus. FN2-CL15 combined with bacterial liquid promoted growth and increased the polysaccharide content of P. umbellatus mycelia. This study reports new bioactive microbial resources for fertilizers or pesticides to enhance the growth and polysaccharide accumulation of P. umbellatus mycelia and offers guidance for exploring the correlation between medicinal macrofungi and associated microbial communities.

With the further development of neural networks, automatic segmentation techniques for melanoma are becoming increasingly mature, especially under the conditions of abundant hardware resources. This allows for the accuracy of segmentation to be improved by increasing the complexity and computational capacity of the model. However, a new problem arises when it comes to actual applications, as there may not be the high-end hardware available, especially in hospitals and among the general public, who may have limited computing resources. In response to this situation, this paper proposes a lightweight deep learning network that can achieve high segmentation accuracy with minimal resource consumption. We introduce a network called DTONet (double-tailed octave network), which was specifically designed for this purpose. Its computational parameter count is only 30,859, which is 1/256th of the mainstream UNet model. Despite its reduced complexity, DTONet demonstrates superior performance in terms of accuracy, with an IOU improvement over other similar models. To validate the generalization capability of this model, we conducted tests on the PH2 dataset, and the results still outperformed existing models. Therefore, the proposed DTONet network exhibits excellent generalization ability and is sufficiently outstanding.

Both the absence of autophagy and excessive autophagy is double-edged sword in tumorigenesis. Due to the specificity of autophagy, its role in head and neck squamous cell carcinoma (HNSCC) is still unclear. In this study, we established five autophagy-related patterns in 1165 HNSCC patients with distinct cellular and molecular characteristics. Additionally, we developed a new scoring system (ATPscore) based on the differentially expressed genes (DEGs) among these five patterns, to represent the individual autophagy regulation pattern. ATPscore was shown to be significantly correlated with tumor immune microenvironment (TIME) infiltration, immune phenotypes, molecular subtypes, and genetic variations. We further found that ATPscore was both an independent prognostic factor and a potent predictor of clinical response to immune-checkpoint inhibitors (ICIs) based immunotherapy. We further verified the value of key gene SRPX in ATPscore in HNSCC cell lines with the in-depth research of ATPscore and found that it is closely related to immune subtypes, molecular subtypes, and immune activation-related markers. Our research could help us to understand the underlying mechanisms of tumor immunity and provide a solid foundation for combination of autophagy-targeted therapies with immunotherapies for clinical application in HNSCC.

Summary: Chronic stress and chronic pain are two major predisposing factors to trigger depression. Enhanced excitatory input to the lateral habenula (LHb) has been implicated in the pathophysiology of depression. However, the contribution of inhibitory transmission remains unclear. Here, we dissect an inhibitory projection from the sensory thalamic reticular nucleus (sTRN) to the LHb, which is activated by acute aversive stimuli. However, chronic restraint stress (CRS) weakens sTRN-LHb synaptic strength, and this synaptic attenuation is indispensable for CRS-induced LHb neural hyperactivity and depression onset. Moreover, artificially inhibiting the sTRN-LHb circuit induces depressive-like behaviors in healthy mice, while enhancing this circuit relieves depression induced by both chronic stress and chronic pain. Intriguingly, neither neuropathic pain nor comorbid mechanical hypersensitivity in chronic stress is affected by this pathway. Altogether, our study demonstrates an sTRN-LHb circuit in establishing and modulating depression, thus shedding light on potential therapeutic targets for preventing or managing depression.

Gut health is important for nutrition absorption, reproduction, and lactation in perinatal and early weaned mammals. Although melatonin functions in maintaining circadian rhythms and preventing obesity, neurodegenerative diseases, and viral infections, its impact on the gut microbiome and its function in mediating gut health through gut microbiota remain largely unexplored. In the present study, the microbiome of rats was monitoring after fecal microbiota transplantation (FMT) and foster care (FC). The results showed that FMT and FC increased intestinal villus height/crypt depth in perinatal rats. Mechanistically, the melatonin-mediated remodeling of gut microbiota inhibited oxidative stress, which led to attenuation of autophagy and inflammation. In addition, FMT and FC encouraged the growth of more beneficial intestinal bacteria, such as Allobaculum, Bifidobacterium, and Faecalibaculum, which produce more short-chain fatty acids to strengthen intestinal anti-oxidation. These findings suggest that melatonin-treated gut microbiota increase the production of SCFAs, which improve gut health by reducing oxidative stress, autophagy and inflammation. The transfer of melatonin-treated gut microbiota may be a new and effective method by which to ameliorate gut health in perinatal and weaned mammals.

Abstract Background Genetic variants can modulate phenotypic outcomes via epigenetic intermediates, for example at methylation quantitative trait loci (mQTL). We present the first large-scale assessment of mQTL at human genomic regions selected for interindividual variation in CpG methylation, which we call correlated regions of systemic interindividual variation (CoRSIVs). These can be assayed in blood DNA and do not reflect interindividual variation in cellular composition. Results We use target-capture bisulfite sequencing to assess DNA methylation at 4086 CoRSIVs in multiple tissues from each of 188 donors in the NIH Gene-Tissue Expression (GTEx) program. At CoRSIVs, DNA methylation in peripheral blood correlates with methylation and gene expression in internal organs. We also discover unprecedented mQTL at these regions. Genetic influences on CoRSIV methylation are extremely strong (median R 2=0.76), cumulatively comprising over 70-fold more human mQTL than detected in the most powerful previous study. Moreover, mQTL beta coefficients at CoRSIVs are highly skewed (i.e., the major allele predicts higher methylation). Both surprising findings are independently validated in a cohort of 47 non-GTEx individuals. Genomic regions flanking CoRSIVs show long-range enrichments for LINE-1 and LTR transposable elements; the skewed beta coefficients may therefore reflect evolutionary selection of genetic variants that promote their methylation and silencing. Analyses of GWAS summary statistics show that mQTL polymorphisms at CoRSIVs are associated with metabolic and other classes of disease. Conclusions A focus on systemic interindividual epigenetic variants, clearly enhanced in mQTL content, should likewise benefit studies attempting to link human epigenetic variation to the risk of disease.

Single-cell RNA sequencing of early to mature adult Drosophila eyes reveals new cell type-specific marker genes and a full set of transcriptomic data for this tissue.

Abstract Heterotopic ossification (HO) is the abnormal formation of bone in extraskeletal sites. However, the mechanisms linking HO pathogenesis with bone mass dysfunction remain unclear. Here, we showed that mice harboring injury-induced and BMP4-dependent HO exhibit bone mass loss similar to that presented by patients with HO. Moreover, we found that injury-induced hyperinflammatory responses at the injury site triggered HO initiation but did not result in bone mass loss at 1 day post-injury (dpi). In contrast, a suppressive immune response promoted HO propagation and bone mass loss by 7 dpi. Correcting immune dysregulation by PD1/PDL1 blockade dramatically alleviated HO propagation and bone mass loss. We further demonstrated that fetuin-A (FetA), which has been frequently detected in HO lesions but rarely observed in HO-adjacent normal bone, acts as an immunomodulator to promote PD1 expression and M2 macrophage polarization, leading to immunosuppression. Intervention with recombinant FetA inhibited hyperinflammation and prevented HO and associated bone mass loss. Collectively, our findings provide new insights into the osteoimmunological interactions that occur during HO formation and suggest that FetA is an immunosuppressor and a potential therapeutic option for the treatment of HO.

The phase separation behaviour of non-structure protein nsp8 of SARS CoV2 in the primer synthesis mechanism is presented, underpinning the replication of coronavirus.

Doxorubicin (DOX) is an extensively used chemotherapeutic agent that can cause severe and frequent cardiotoxicity, which limits its clinical application. Although there have been extensive researches on the cardiotoxicity caused by DOX, there is still a lack of effective treatment. It is necessary to understand the molecular mechanism of DOX-induced cardiotoxicity and search for new therapeutic targets which do not sacrifice their anticancer effects. Mitochondria are considered to be the main target of cardiotoxicity caused by DOX. The imbalance of mitochondrial dynamics characterized by increased mitochondrial fission and inhibited mitochondrial fusion is often reported in DOX-induced cardiotoxicity, which can result in excessive ROS production, energy metabolism disorders, cell apoptosis, and various other problems. Also, mitochondrial dynamics disorder is related to tumorigenesis. Surprisingly, recent studies show that targeting mitochondrial dynamics proteins such as DRP1 and MFN2 can not only defend against DOX-induced cardiotoxicity but also enhance or not impair the anticancer effect. Herein, we summarize mitochondrial dynamics disorder in DOX-induced cardiac injury. Furthermore, we provide an overview of current pharmacological and non-pharmacological interventions targeting proteins involved in mitochondrial dynamics to alleviate cardiac damage caused by DOX.

Oxidative stress (OS), defined as redox imbalance in favor of oxidant burden, is one of the most significant biological events in cancer progression. Cancer cells generally represent a higher oxidant level, which suggests a dual therapeutic strategy by regulating redox status (i.e., pro-oxidant therapy and/or antioxidant therapy). Indeed, pro-oxidant therapy exhibits a great anti-cancer capability, attributing to a higher oxidant accumulation within cancer cells, whereas antioxidant therapy to restore redox homeostasis has been claimed to fail in several clinical practices. Targeting the redox vulnerability of cancer cells by pro-oxidants capable of generating excessive reactive oxygen species (ROS) has surfaced as an important anti-cancer strategy. However, multiple adverse effects caused by the indiscriminate attacks of uncontrolled drug-induced OS on normal tissues and the drug-tolerant capacity of some certain cancer cells greatly limit their further applications. Herein, we review several representative oxidative anti-cancer drugs and summarize their side effects on normal tissues and organs, emphasizing that seeking a balance between pro-oxidant therapy and oxidative damage is of great value in exploiting next-generation OS-based anti-cancer chemotherapeutics.

The increasing global demand for skin disease diagnostics emphasizes the urgent need for advancements in AI-assisted diagnostic technologies for dermatoscopic images. In current practical medical systems, the primary challenge is balancing lightweight models with accurate image analysis to address constraints like limited storage and computational costs. While knowledge distillation methods hold immense potential in healthcare applications, related research on multi-class skin disease tasks is scarce. To bridge this gap, our study introduces an enhanced multi-source knowledge fusion distillation framework, termed DSP-KD, which improves knowledge transfer in a dual-stage progressive distillation approach to maximize mutual information between teacher and student representations. The experimental results highlight the superior performance of our distilled ShuffleNetV2 on both the ISIC2019 dataset and our private skin disorders dataset. Compared to other state-of-the-art distillation methods using diverse knowledge sources, the DSP-KD demonstrates remarkable effectiveness with a smaller computational burden.

Pancreatic stellate cells (PSCs) are the primary cell components of pancreatic cancer (PC) and are involved in tumor growth, metastasis and resistance. However, the role and the mechanism of PSCs in gemcitabine (GEM) resistance to PC still need more investigation. We found that CXCL12 mRNA and secreted CXCL12 protein were higher in PSCs after GEM treatment. The conditioned medium (CM) from GEM-treated PSCs reduced the GEM sensitivity of PC cells. Blocking of CXCL12 in CM by anti-CXCL12 antibody partly restored the GEM sensitivity of PC cells. Blocking of CXCL12 decreased glucose consumption, lactate production, ECAR, and glycolysis-related gene expression in PC cells. The PI3K/AKT/mTOR pathway was activated by the binding of CXCL12 and CXCR4. Moreover, CXCR4 mRNA and protein expressions in PC cells were increased after GEM treatment. Our results indicated the cross-talk between PSCs and PC cells during GEM chemotherapy. CXCL12 secreted by PSCs reduces GEM sensitivity of PC cells by binding to CXCR4 and activating PI3K/AKT/mTOR-glycolysis pathway in PC. Our findings would lay the foundation for solving GEM resistance in PC.

Neural crest-derived cells play essential roles in skin function and homeostasis. However, how they interact with environmental cues and differentiate into functional skin cells remains unclear. Using a combination of single-cell data analysis, neural crest lineage tracing, and flow cytometry, we found that the expression of integrin α6 (ITGA6) in neural crest and its derivatives was developmentally regulated and that ITGA6 could serve as a functional surface marker for distinguishing neural crest derivatives in the skin. Based on the expression of ITGA6, Wnt1-Cre lineage neural crest derivatives in the skin could be categorized into three subpopulations, namely, ITGA6bright, ITGA6dim, and ITGA6neg, which were found to be Schwann cells, melanocytes, and fibroblasts, respectively. We further analyzed the signature genes and transcription factors that specifically enriched in each cell subpopulation, as well as the ligand or receptor molecules, mediating the potential interaction with other cells of the skin. Additionally, we found that Hmx1 and Lhx8 are specifically expressed in neural crest-derived fibroblasts, while Zic1 and homeobox family genes are expressed in mesoderm-derived fibroblasts, indicating the distinct development pathways of fibroblasts of different origins. Our study provides insights into the regulatory landscape of neural crest cell development and identifies potential markers that facilitate the isolation of different neural crest derivatives in the skin.

Summary: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has had a tremendous impact worldwide. Mapping virus-host interactions is critical to understand disease progression. MicroRNAs (miRNAs) are important RNA regulators, but their interaction with SARS-CoV-2 RNA was not experimentally investigated. Here, using Argonaute (AGO) cross-linking immunoprecipitation combined with RNA proximity ligation (CLEAR-CLIP), we provide unbiased mapping of SARS-CoV-2/miRNA interactions. We identified six main regions on the viral RNA bound primarily by one specific miRNA. Targeted mutagenesis and AGO1-3 knockdown demonstrated that these interactions are not critical for virus production. Moreover, we identified perturbed regulation of cellular miRNA interactions during infection, including non-compensated viral sequestration of the miR-15 family. Transcriptome analysis further showed that mRNAs targeted by this miRNA family are derepressed. This work delineates the interphase between miRNA regulation and SARS-CoV-2 infection and further contributes to deciphering the full molecular interactome of this virus.

Summary: Branched-chain amino acids (BCAAs) provide nutrient signals for cell survival and growth. How BCAAs affect CD8+ T cell functions remains unexplored. Herein, we report that accumulation of BCAAs in CD8+ T cells due to the impairment of BCAA degradation in 2C-type serine/threonine protein phosphatase (PP2Cm)-deficient mice leads to hyper-activity of CD8+ T cells and enhanced anti-tumor immunity. CD8+ T cells from PP2Cm−/− mice upregulate glucose transporter Glut1 expression in a FoxO1-dependent manner with more glucose uptake, as well as increased glycolysis and oxidative phosphorylation. Moreover, BCAA supplementation recapitulates CD8+ T cell hyper-functions and synergizes with anti-PD-1, in line with a better prognosis in NSCLC patients containing high BCAAs when receiving anti-PD-1 therapy. Our finding thus reveals that accumulation of BCAAs promotes effector function and anti-tumor immunity of CD8+ T cells through reprogramming glucose metabolism, making BCAAs alternative supplementary components to increase the clinical efficacy of anti-PD-1 immunotherapy against tumors.

Abstract Integration of single-cell multiomics profiles generated by different single-cell technologies from the same biological sample is still challenging. Previous approaches based on shared features have only provided approximate solutions. Here, we present a novel mathematical solution named bi-order canonical correlation analysis (bi-CCA), which extends the widely used CCA approach to iteratively align the rows and the columns between data matrices. Bi-CCA is generally applicable to combinations of any two single-cell modalities. Validations using co-assayed ground truth data and application to a CAR-NK study and a fetal muscle atlas demonstrate its capability in generating accurate multimodal co-embeddings and discovering cellular identity.

Abstract Background Autism spectrum disorder (ASD) is a group of complex neurodevelopment disorders with a strong genetic basis. Large scale sequencing studies have identified over one hundred ASD risk genes. Nevertheless, the vast majority of ASD risk genes remain to be discovered, as it is estimated that more than 1000 genes are likely to be involved in ASD risk. Prioritization of risk genes is an effective strategy to increase the power of identifying novel risk genes in genetics studies of ASD. As ASD risk genes are likely to exhibit distinct properties from multiple angles, we reason that integrating multiple levels of genomic data is a powerful approach to pinpoint genuine ASD risk genes. Results We present BNScore, a Bayesian model selection framework to probabilistically prioritize ASD risk genes through explicitly integrating evidence from sequencing-identified ASD genes, biological annotations, and gene functional network. We demonstrate the validity of our approach and its improved performance over existing methods by examining the resulting top candidate ASD risk genes against sets of high-confidence benchmark genes and large-scale ASD genome-wide association studies. We assess the tissue-, cell type- and development stage-specific expression properties of top prioritized genes, and find strong expression specificity in brain tissues, striatal medium spiny neurons, and fetal developmental stages. Conclusions In summary, we show that by integrating sequencing findings, functional annotation profiles, and gene-gene functional network, our proposed BNScore provides competitive performance compared to current state-of-the-art methods in prioritizing ASD genes. Our method offers a general and flexible strategy to risk gene prioritization that can potentially be applied to other complex traits as well.

Quality control procedures in the manufacturing of tableware ceramics require a demanding, monotonous, subjective, and faulty human manual inspection. This paper presents two machine learning strategies and the results of a semi-automated visual inspection of ceramics tableware applied to a private dataset acquired during the VAICeramics project. In one method, an anomaly detection step was integrated to pre-select possible defective patches before passing through an object detector and defects classifier. In the alternative one, all patches are directly provided to the object detector and then go through the classification phase. Contrary to expectations, the inclusion of the anomaly detector demonstrated a slight reduction in the performance of the pipeline, which may result from error propagation. Regarding the proposed methodology for defect detection, it exhibits average performance in monochromatic images with more than 600 real defects in total, efficiently identifying the most common defect classes in highly reflective surfaces. However, when applied to newly acquired images, the pipeline encounters challenges revealing a lack of generalization ability and experiencing limitations in detecting specific defect classes, due to their appearance and limited available samples used for training. Only two defect types presented high classification performance, namely Dots and Cracked defects.

The measurement of soil gas permeability is influenced by the temperature and pressure fluctuation in the low gas pressure region. In order to investigate these influences, a soil temperature-controlled apparatus connected to a low-gas-pressure supply equipment is proposed in this study. The low constant gas pressure is supplied by two Mariotte bottles, by which the airflow rate is measured. Meanwhile, the soil specimen is controlled by a temperature-controlled apparatus. During the test, the negative pore water pressure and volume change of the soil specimen are measured. Through the temperature-controlled apparatus, it is observed that as the temperature increases from 25 °C to 60 °C, there is a corresponding increase in soil sample porosity by 5.4%, while the negative pressure of pore water decreases by 11.1%. This can be attributed to the reduction in the surface tension of contractile skin caused by elevated temperatures. Furthermore, due to variations in gas viscosity with temperature, there was a significant decrease in the gas flow rate by 50.5%. And, the relationship between permeability and volumetric gas content at different temperatures in low-pressure regions well confirms the existing power-law model. In addition, the existence of a temperature-independent critical negative pore water pressure is observed, beyond which the intrinsic permeability remains constant. At 36 kPa of negative pore water pressure, the intrinsic permeability at 60 °C exhibits an 81.8% reduction compared to that at 25 °C. This decline in intrinsic permeability can be attributed to a diminished pore connectivity, resulting from elevated temperatures.

Phenanthrene (PHE) is one of the model compounds of polycyclic aromatic hydrocarbons (PAHs). In this study, a natural PHE-degrading microbial consortium, named HJ-SH, with very high degradation efficiency was isolated from soil exposed to long-term PHE contamination. The results of GC analysis showed that the consortium HJ-SH degraded 98% of 100 mg/L PHE in 3 days and 93% of 1000 mg/L PHE in 5 days, an efficiency higher than that of any other natural consortia, and even most of the engineered strains and consortia reported so far. Seven dominating strains were isolated from the microbial consortium HJ-SH, named SH-1 to SH-7, which were identified according to morphological observation and 16S rDNA sequencing as Pseudomonas sp., Stenotrophomonas sp., Delftia sp., Pseudomonas sp., Brevundimonas sp., Curtobacterium sp., and Microbacterium sp., respectively. Among all the seven single strains, SH-4 showed the strongest PHE degradation ability, and had the biggest degradation contribution. However, it is very interesting that the microbial consortium can hold its high degradation ability only with the co-existence of all these seven single strains. Moreover, HJ-SH exhibited a very high tolerance for PHE, up to 4.5 g/L, and it can degrade some other typical organic pollutants such as biphenyl, anthracene, and n-hexadecane with the degradation ratios of 93%, 92% and 70%, respectively, under 100 mg/L initial concentration in 5 days. Then, we constructed an artificial consortium HJ-7 consisting of the seven single strains, SH-1 to SH-7. After comparing the degradation ratios, cell growth, and relative degradation rates, it was concluded that the artificial consortium HJ-7 with easier reproducibility, better application stability, and larger room for modification can largely replace the natural consortium HJ-SH. In conclusion, this research provided novel tools and new insights for the bioremediation of PHE and other typical organic pollutants using microbial consortia.

Background Bud sport mutation occurs frequently in fruit plants and acts as an important approach for grapevine improvement and breeding. ‘Jinzao Wuhe’ is a bud sport of the elite cultivar ‘Himord Seedless’ with obviously enlarged organs and berries. To date, the molecular mechanisms underlying berry enlargement caused by bud sport in grapevines remain unclear. Methods Whole genome resequencing (WGRS) was performed for two pairs of bud sports and their maternal plants with similar phenotype to identify SNPs, InDels and structural variations (SVs) as well as related genes. Furthermore, transcriptomic sequencing at different developmental stages and weighted gene co-expression network analysis (WGCNA) for ‘Jinzao Wuhe’ and its maternal plant ‘Himord Seedless’ were carried out to identify the differentially expressed genes (DEGs), which were subsequently analyzed for Gene Ontology (GO) and function annotation. Results In two pairs of enlarged berry bud sports, a total of 1,334 SNPs, 272 InDels and 74 SVs, corresponding to 1,022 target genes related to symbiotic microorganisms, cell death and other processes were identified. Meanwhile, 1,149 DEGs associated with cell wall modification, stress-response and cell killing might be responsible for the phenotypic variation were also determined. As a result, 42 DEGs between ‘Himord Seedless’ and ‘Jinzao Wuhe’ harboring genetic variations were further investigated, including pectin esterase, cellulase A, cytochromes P450 (CYP), UDP-glycosyltransferase (UGT), zinc finger protein, auxin response factor (ARF), NAC transcription factor (TF), protein kinase, etc. These candidate genes offer important clues for a better understanding of developmental regulations of berry enlargement in grapevine. Conclusion Our results provide candidate genes and valuable information for dissecting the underlying mechanisms of berry development and contribute to future improvement of grapevine cultivars.