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Chai, B.

Publications and source records attributed to Chai, B..

11 recordsLinked to original sources

Stain Normalisation Does Not Consistently Improve Matched-Location Retrieval with Pathology Foundation Models

Pathology foundation models provide reusable representations for computational pathology, but staining- and scanner-induced variation may compromise the robustness and reproducibility of embedding-based analyses across acquisition settings. Stain normalisation is widely used to mitigate such colour variation, yet whether it improves retrieval with modern self-supervised pathology encoders remains unclear. We test whether stain normalisation improves cross-scanner and cross-staining image retrieval using the PLISM whole-slide image subset, comprising 13 co-registered images of serial sections prepared under different staining conditions and digitised using seven scanners (91 whole-slide images). We sample 400 matched locations across the 91 images, yielding 36,400 tile instances. We compare two DINOv2-based encoders, Phikon-v2 (1,024-dimensional) and Midnight-12k (3,072-dimensional), with Reinhard and Macenko normalisation against an unnormalised baseline. Performance is measured using paired top-1 nearest-neighbour retrieval accuracy in two settings: cross-scanner retrieval of the same physical section digitised by different scanners, and cross-staining retrieval across co-registered images of serial sections, which differ in staining condition and may also contain section-level morphological variation. Neither normalisation method consistently improves top-1 retrieval relative to no normalisation, while Macenko reduces accuracy by up to 18.3 percentage points. An exploratory UMAP of unnormalised Midnight-12k slide-level mean embeddings showed partial overlap between scanner groups in a two-dimensional projection. These results challenge the routine use of stain normalisation in foundation-model retrieval pipelines and support validating preprocessing choices for each encoder and retrieval setting.

pathology↗

Pheno-MYCN maps the morphological footprint of MYCN amplification in paediatric neuroblastoma

MYCN amplification has long been a prognostic marker in paediatric neuroblastoma, yet is typically assayed in bulk, alongside rather than within the heterogeneous tissue architecture pathologists assess. This leaves a gap: MYCN status alone cannot localise MYCN-associated biology, while morphology alone cannot assign molecular risk. Motivated by our finding that the two together identify high-risk cases missed by either, we developed Pheno-MYCN, a weakly supervised framework linking slide-level MYCN prediction to interpretable morphological sub-populations on routine H&E whole-slide images. The aim is not a stronger classifier: prediction probes what MYCN amplification does to the tissue, its evidence open to pathological scrutiny. Across 189 slides, Pheno-MYCN resolved each into phenotypic clusters that expert review mapped to neuroblastoma morphologies. Cell-level profiling revealed MYCN amplification "marked" every sub-population, through a different feature in each: densely cellular yet disorganised tumour with sparser, less diverse networks; chiefly abundance in necrotic and haemorrhagic regions. MYCN-amplified-like tissue was identifiable per slide from these features alone (AUC 0.93-1.00, leave-one-slide-out) and traced as a continuous gradient within tumours. Thus MYCN amplification leaves a concrete, interpretable footprint that can be read and localised on routine H&E, offering a low-cost means to flag and map it where molecular testing is limited.

cancer biology↗

A Course-Undergraduate Research Experience (CURE) to explore the effect of structural variants on gene expression in C. elegans balancers

Bioinformatics, a discipline at the crossroads of Biology and Computational Sciences, also referred to as Computational Biology, is nowadays widely spread in research programs. However, implementing any Bioinformatics projects requires the ability to comprehend biological concepts and apply computational approaches, and rare are the undergraduate programs offering such multi-disciplinary training. In addition, understanding the dynamic between Biology research projects and Bioinformatics analyses is challenging with no real-life experience. Course-based undergraduate research experience (CURE) courses are innovative programs that allow more students to acquire research experience and provide the perfect setting to introduce students to applied bioinformatics. As a part of the Bachelor of Health Sciences of the Cumming School of Medicine at the University of Calgary (Canada), a CURE applied bioinformatics was implemented in the Winter of 2023 to 2025. Students investigated the effect of structural variants (SVs, genetic variants larger than 50 bp) on gene expression in the model organism Caenorhabditis elegans (a hermaphrodite 1-mm long roundworm). The students detected and characterized SVs by analyzing genome and transcriptome sequencing data of C. elegans strains called balancers, as they are known to carry large genomic variations balancing regions of the genome by limiting recombination and allowing maintenance of lethal mutations. They used Galaxy, a public web-based supercomputing resource, but also a local High-Performance computing system, and R, to report different effects of SVs on gene expression and splicing. Students research explained the molecular mechanism behind the uncoordinated phenotype caused by the reciprocal translocation eT1(III;V) and uncovered unexpected effects on gene expression on an understudied gene. We evaluated the courses impact on student learning journeys and showed that the CURE favored students understanding of the Bioinformatics field and fostered their research interest. We provide here guidelines to facilitate the CURE implementations to improve access for undergraduate students to bioinformatics research experiences.

bioinformatics↗

Impact of variation in tissue staining and scanning devices on performance of pan-cancer AI models: a study of sarcoma and their mimics

Histopathological analysis is considered the gold standard for the diagnosis and prognostication of cancer. Recent advances in AI, driven by large-scale digitisation and pan-cancer foundation models, are opening new opportunities for clinical integration. However, it remains unclear how robust these foundation models are to real-world sources of variability, particularly in H&E staining and scanning protocols. In this study, we use soft tissue tumours, a rare and morphologically diverse tumour type, as a challenging test case to systematically investigate the colour-related robustness and generalisability of seven AI models. Controlled staining and scanning experiments were utilised to assess model performance across diverse real-world data sources. Foundation models, particularly UNI-v2, Virchow and TITAN, demonstrated encouraging robustness to staining and scanning variation, particularly when a small number of stain-varied slides were included in the training loop, highlighting their potential as adaptable and data-efficient tools for real-world digital pathology workflows.

pathology↗

Multi-SpinX: An Advanced Framework for Automated Tracking of Mitotic Spindles and Kinetochores in Multicellular Environments

SpinX, an AI-guided spindle tracking software, allows the 3-dimensional (3D) tracking of metaphase spindle movements in mammalian cells. Using over 900 images of dividing cells, we create the Multi-SpinX framework to significantly expand SpinXs applications: a) to track spindles and cell cortex in multicellular environments, b) to combine two object tracking (spindle with kinetochores marked by centromeric probes) and c) to extend spindle tracking beyond metaphase to prometaphase and anaphase stages where spindle morphology is different. We have used a human-in-the-loop approach to assess our optimisation steps, to manually identify challenges and to build a robust computational pipeline for segmenting kinetochore pairs and spindles. Spindles of both H1299 and RPE1 cells have been assessed and validated for use through Multi-SpinX, and we expect the tool to be versatile in enabling quantitative studies of mitotic subcellular dynamics.

cell biology↗

Development of a ferritin-based nanoparticle vaccine against the SARS-CoV-2 Omicron variant

A new SARS-CoV-2 variant named Omicron (B.1.1.529) discovered initially in South Africa has recently been proposed as a variant of concern (VOC) by the World Health Organization, because of its high transmissibility and resistance to current vaccines and therapeutic antibodies. Therefore, rapid development of vaccines against prevalent variants including Omicron is urgently needed for COVID-19 prevention. Here, we designed a self-assembling ferritin-based nanoparticle (FNP) vaccine against the SARS-CoV-2 Omicron variant. The purified Fc-RBDOmicron automatically formed a dimer depending on the nature of the Fc tag, thus assembling onto the nanoparticles by the Fc-protein A tag interaction (FNP-Fc-RBDOmicron). The results of hACE2-transgenic mice immunization showed that SARS-CoV-2 Omicron RBD-specific IgG titer induced by FNP-Fc-RBDOmicron was much higher than that by Fc-RBDOmicron. Consistently, the sera showed a higher neutralizing activity against SARS-CoV-2 Omicron BA.1 and BA.2 in the FNP-Fc-RBDOmicron immunized mice, indicating that immunization of a self-assembling ferritin-based nanoparticle vaccine offers a robust humoral immune response against Omicron variants. This study offers a great potential for the quick response of the emerging SARS-CoV-2 variants and affords versatility to develop universal vaccines against other emerging and reemerging coronaviruses in the future.

microbiology↗

The human disease gene CLEC16A encodes an intrinsically disordered protein region required for mitochondrial quality control

CLEC16A regulates mitochondrial health through mitophagy and is associated with over 20 human diseases. While CLEC16A has ubiquitin ligase activity, the key structural and functional regions of CLEC16A, and their relevance for human disease, remain unknown. Here, we report that a disease-associated CLEC16A variant lacks a C-terminal intrinsically disordered protein region (IDPR) that is critical for mitochondrial quality control. Using carbon detect NMR, we find that the CLEC16A C terminus lacks secondary structure, validating the presence of an IDPR. Loss of the CLEC16A C-terminal IDPR in vivo impairs pancreatic {beta}-cell mitophagy, mitochondrial function, and glucose-stimulated insulin secretion, ultimately causing glucose intolerance. Deletion of the CLEC16A C-terminal IDPR increases its self-ubiquitination and destabilizes CLEC16A, thus impairing formation of a critical CLEC16A-dependent mitophagy complex. Importantly, CLEC16A stability is dependent on proline bias within the C-terminal IDPR, but not amino acid sequence order or charge. Together, we clarify how an IDPR in CLEC16A prevents diabetes, thus implicating the disruption of IDPRs as novel pathological contributors to diabetes and other CLEC16A-associated diseases.

molecular biology↗

Mitophagy protects beta cells from inflammatory damage in diabetes

Inflammatory damage contributes to {beta}-cell failure in type 1 and 2 diabetes (T1D and T2D). Mitochondria are damaged by inflammatory signaling in {beta}-cells, resulting in impaired bioenergetics and initiation of pro-apoptotic machinery. Hence, the identification of protective responses to inflammation could lead to new therapeutic targets. Here we report that mitophagy serves as a protective response to inflammatory stress in both human and rodent {beta}-cells. Utilizing in vivo mitophagy reporters, we observed that diabetogenic pro-inflammatory cytokines induced mitophagy in response to nitrosative/oxidative mitochondrial damage. Mitophagy-deficient {beta}-cells were sensitized to inflammatory stress, leading to the accumulation of fragmented dysfunctional mitochondria, increased {beta}-cell death, and hyperglycemia. Overexpression of CLEC16A, a T1D gene and mitophagy regulator whose expression in islets is protective against T1D, ameliorated cytokine-induced human {beta}-cell apoptosis. Thus, mitophagy promotes {beta}-cell survival and prevents diabetes by countering inflammatory injury. Targeting this pathway has the potential to prevent {beta}-cell failure in diabetes and may be beneficial in other inflammatory conditions.

cell biology↗

Distribution Pattern and Diversity Maintenance Mechanism of the Denitrifier Community in Alkaline Copper Mine Drainage

Denitrifiers have been shown to vary in abundance and diversity across the environmental gradients; however, the factors that determine the type and magnitude of the response of the denitrifier communities remain unclear. In order to reveal the effects of alkaline mine drainage (AlkMD) on the denitrifier community composition and diversity maintenance mechanism in a tailings reservoir, we examined the diversity patterns and adaptation mechanisms of different denitrifier communities in Shibahe copper tailings water in Zhongtiaoshan, China. The results showed that the -diversity of Proteobacteria and the nosZI-bearing denitrifier community in downstream seeping water (SDSW) were the highest, while those in the upstream tailings water (STW1) were the lowest. The highest nirS and nirK-bearing denitrifier community -diversity were measured in STW1, and the lowest in STW3. The community dissimilarity of the denitrifier communities was strongly correlated with environment parameters, but the factors varied in different groups. The Proteobacteria community was correlated strongly with nitrate (NO3-); the nirS and nirK-bearing denitrifier communities were correlated strongly with pH, total carbon (TC), NO3- and ammonia nitrogen (NH4+), and the nosZI-bearing denitrifier community was correlated strongly with total organic carbon (TOC), dissolved oxygen (DO), NO3-, electroconductibility (EC) and spatial distance (PCNM1). Our results indicated that environmental changes were valuable index reflecting variations in denitrifier community composition in AlkMD. Additionally, the findings in this study are helpful in understanding the relationship between the microbial community composition changes and functional adaptation in different ecosystems. IMPORTANCEMetal mine tailings pond is an important site polluted by heavy metals and nitrogen, and excess nitrogen is mainly removed by microorganisms through denitrification. Although many studies have reported that Proteobacteria is the main denitrifying bacteria, and nirS, nirK and nosZ-bearing denitrifiers are three key functional groups in denitrification process. However, less is known of their response to discharge of alkaline copper tailings wastewater (AlkMD). AlkMD exerts an adverse impact on composition and structure of denitrifying bacteria community. The change of nitrogen and carbon concentration along the flow direction of wastewater resulted in the change of denitrifying bacteria community diversity pattern, that is to say, environmental filtering force drove the denitrifier community structure in this highly polluted ecosystem.

microbiology↗

Antibacterial activity of total flavonoids from Ilex rotunda Thunb. and different antibacterials on different multidrug-resistant bacteria alone or in combination

The problem of bacterial resistance is becoming more and more serious, which has become an urgent problem to be solved in human and veterinary. One approach to control and delay bacterial resistance is combination therapy in which antibiotics are given together with other antimicrobial or non-antimicrobial agents. Studies have shown that flavonoids from Traditional Chinese medicine (TCM) possess a high level of antibacterial activity against antibiotic resistant strains. The aim of this study was to evaluate the antibacterial effects of a combined therapy of total flavonoids from Ilex rotunda Thunb. and antibiotics against seven kinds of veterinary bacteria which were multidrug resistance bacteria. A microdilution checkerboard method was used to determine the minimal inhibitory concentrations of both types of antimicrobials, alone and in combination. The fractional inhibitory concentration index was calculated and used to classify observed collective antibacterial activity as synergistic, additive, indifferent or antagonistic.\n\nFrom the performed tests, the total flavonoids and antimicrobial agents were combined to inhibit different multidrug-resistant bacteria, such as Escherichia coli, Streptococcus, Pseudomonas aeruginosa, Enterococcus faecalis, Proteus vulgaris, Staphylococcus aureus, Acinetobacter baumannii. For these bacteria, total flavonoids from Ilex Rotunda Thunb. presented synergistic or additive with different antibiotics and had a certain antibacterial effect on the separated multidrug-resistant bacteria. The study shows total flavonoids from Ilex rotunda Thunb. have potential as adjuvants for the treatment of animal bacterial diseases.

microbiology↗

4-hydroxyphenylpyruvate dioxygenase thermolability is responsible for temperature-dependent melanogenesis in Aeromonas salmonicida subsP salmonicida

Aeromonas salmonicida subsp. salmonicida (A.s.s) is a major pathogen affecting fisheries worldwide. It is a well-known member of the pigmented Aeromonas species, which produces melanin at [≤] 22 {degrees}C. However, melanogenesis decreases as the culture temperature increases and is completely suppressed at 30-35 {degrees}C while bacterial growth is not affected. The mechanism and biological significance of this temperature-dependent melanogenesis are not clear. Heterologous expression of an A.s.s. 4-hydroxyphenylpyruvate dioxygenase (HppD), the most crucial enzyme in the HGA-melanin synthesis pathway, results in thermosensitive pigmentation in Escherichia coli, suggesting that HppD plays a key role in this process. In the current study, we demonstrated that the extreme thermolability of HppD is responsible for the temperature-dependent melanization of A.s.s. Substitutions in three residues, Ser18, Pro103, or Leu119 of HppD from A.s.s increases the thermolability of this enzyme and results in temperature-independent melanogenesis. Moreover, replacing the corresponding residues of HppD from Aeromonas media strain WS, which forms pigment independent of temperature, with those of A.s.s HppD leads to thermosensitive melanogenesis. Structural analysis suggested that mutations at these sites, especially at position P103, can strengthen the secondary structure of HppD and greatly improve its thermal stability. In addition, we found that HppD sequences of all A.s.s isolates are identical and that two of the three residues are completely conserved within A.s.s isolates, which clearly distinguishes these from other Aeromonas strains. We suggest that this property represents an adaptive strategy to the psychrophilic lifestyle of A.s.s.\n\nImportanceAeromonas salmonicida subsp. salmonicida (A.s.s) is the causative agent of furunculosis, a bacterial septicemia of cold water fish of the Salmonidae family. As it has a well-defined host range, A.s.s has become an ideal model to investigate the co-evolution of host and pathogen. For many pathogens, melanin production is associated with virulence. Although other species of Aeromonas can produce melanin, A.s.s is the only member of this genus that has been reported to exhibit temperature-dependent melanization. Here we demonstrate that thermosensitive melanogenesis in A.s.s strains is due to the thermolability of 4-hydroxyphenylpyruvate dioxygenase (HppD). The strictly conserved hppD sequences among A.s.s and the exclusive thermosensitive pigmentation of these strains might provide insight into the role of melanin in the adaptation to a particular host, and offer a novel molecular marker to readily differentiate A.s.s strains from other A. salmonicida subspecies and Aeromonas species.

molecular biology↗