Biology subjects

Haque, N.

Publications and source records attributed to Haque, N..

17 recordsLinked to original sources

bioRxiv2026

Defining Pseudo-Haplotype Analysis Reveals Multi-Gene Genetic Pattern Across BAF Chromatin Remodeling Complexes

BRG1-associated factor (BAF) is a crucial chromatin remodeling complex. Variants in genes encoding BAF complex components cause human diseases, including cancers and developmental disorders. However, the genetic diversity and variant co-occurrence patterns within BAF genes remain incompletely understood. It is feasible, though largely untested, that rare patterns of common variations could alter function similarly to rare deleterious variants. Further, there is no modern census of how often individual people simultaneously carry multiple rare and common variations, nor means for genomics practitioners to assess their combined effects. Approaches are needed to characterize complete sequences from individual samples. In this study, we introduce a pseudo-haplotype analysis (PHA) framework, combining multiple protein-coding sequence variants, observed concurrently within individual samples, into discrete BAF patterns. In this cohort, 78.44% of pseudo-haplotype (PH) copies carry at least one BAF coding variation. Among these, 56.18% contain at least two distinct variants, and 32.39% contain three or more, indicating a substantial burden of multi-variant configurations across individuals. Notably, 25.30% of unique PHs are observed only once, highlighting a considerable proportion of people who are affected by rare or private combinations of genetic variations. We identify multiple significant (FDR < 0.05) co-occurrence combinations across global populations. These findings underscore the importance of considering population-specific genetic structures, and complete individual variant configurations when investigating disease associations and genetic mechanisms. Our approach provides a generalizable framework for characterizing multi-variant architectures within chromatin remodeling genes at a population scale, with potential applications in elucidating disease etiology and advancing precision medicine.

bioinformatics↗

bioRxiv2026

ARID1B damaging variants from more than one million genomes, cause human diseases by impairing protein-protein interactions, stability, and regulation

ARID1B is the most frequently de novo altered gene across a spectrum of human neurodevelopmental disorders and cancers. We found 1,456 missense variants in ARID1Bs C-terminal domains, 94% of which are clinically uninterpreted and 59% of which are observed in human disorders and cancers. Using integrative modeling of ARID1B cBAF and DNA bound structures, we calculate how these variants impact key functional sites, structural stability, and topological features, finding that 617 variants clearly impair ARID1Bs interactions within BAF, interactions with DNA, fold stability, or post-translational regulation. Our study enables scalable and precise variant interpretation by illuminating the molecular mechanisms by which missense variants damage ARID1B function, with commonalities across malignancies and congenital anomalies mutually informing therapeutic developments.

genetics↗

bioRxiv2026

TF-IDF k-mer-based Classical and Hybrid Machine Learning Models for SARS-CoV-2 Variant Classification under Imbalanced Genomic Data

Accurate classification of SARS-CoV-2 genomic variants is essential for effective genomic surveillance, yet it is challenged by extreme class imbalance, limited representation of rare variants, and distribution shifts in real-world sequencing data. In this study, we employed hybrid RF-SVM framework designed for robust detection of rare SARS-CoV-2 variants. It integrates a random forest and a polynomial-kernel based support vector machine to enhance sensitivity to minority classes while maintaining overall predictive stability. We systematically compared classical machine learning models, deep learning approaches, and hybrid strategies under both standard and distribution-shifted evaluation settings. Our results show that classical models using TF-IDF-based k-mer features outperform deep learning methods on macro-averaged performance metrics. The Random Forest classifier using TF-IDF Feature achieved the best overall performance, with a macro-averaged F1-score of 0.8894 and an accuracy of 96.3%. The model also demonstrated strong generalization ability, as evidenced by stable cross-validation performance (CV accuracy = 0.9637). Hybrid RF-SVM model further improves rare variant detection under severe class imbalance. Calibration analysis indicates reliable probability estimates for common variants, although challenges persist for minority classes. Overall, this study highlights the limitations of deep learning in highly imbalanced genomic settings and demonstrates that carefully designed hybrid machine learning approaches provide an effective and interpretable solution for rare SARS-CoV-2 variant detection.

bioinformatics↗

bioRxiv2026

Transitory enhancement of GATA2 chromatin engagement during early erythroid differentiation

Erythroid differentiation requires precise regulation of transcription factor binding to chromatin targets as hematopoietic progenitors relinquish multipotency and activate lineage programs. GATA2 maintains progenitor identity and is thought to be progressively silenced as GATA1 levels rise; however, the precise changes in GATA2 chromatin binding kinetics during this transition remain undefined. Here, we combined live-cell single-molecule imaging in cell lines and primary mouse progenitors with CUT&Tag chromatin profiling to define GATA2 activity during erythropoiesis. Single-molecule tracking resolved two interaction modes: short-lived (<1 s) searching interactions and long-lived (>5 s) binding. Surprisingly, early erythroid differentiation was characterized by a transitory strengthening of long-lived GATA2 chromatin engagement. This manifested as increased residence time of GATA2 bound to chromatin in G1E-ER4 cells and an expansion of the long-lived bound population in HPC7 cells and primary mouse progenitors. This transitory phase of enhanced engagement declined upon further differentiation. Genome-wide mapping identified regulatory elements selectively occupied by GATA2 during this early transition state, revealing promoter-proximal sites enriched for GATA/RUNX motifs and distal elements containing composite GATA/E-box signatures. Together, our imaging and chromatin profiling indicate that GATA2 chromatin engagement is kinetically remodeled at the onset of differentiation, with early recruitment targets partitioning into distinct promoter- and enhancer-associated subclasses. These results support a model in which transcription factor kinetics constitute a dynamic chromatin engagement layer that characterizes the GATA2-to-GATA1 transition.

cell biology↗

bioRxiv2026

Heavy Metal-Resistant, Plastic-Degrading Bacillus sp. Isolated from Landfill Leachate: Identification and Characterization

Landfill leachates in rapidly urbanizing regions like Dhaka present a complex ecological challenge owing to the concurrent buildup of heavy metals and plastic waste. Despite the severity of this pollution, the role of indigenous multi-functional bacteria in mitigating these mixed contaminants remains poorly understood. This research sought to isolate and characterize bacteria resistant to heavy metals and capable of degrading plastics from the Aminbazar and Matuail landfills and evaluate their bioremediation potential. Physicochemical analysis confirmed extreme contamination, with heavy metal levels (Pb, Cr, Cd, Cu) significantly exceeding WHO safety limits. Out of 81 isolates, nearly half exhibited multi-metal resistance and polyethylene (PE) degradation capacity. Statistical analysis showed a significant correlation between plastic degradation and multi-metal tolerance, suggesting a linked evolutionary adaptation. Enzymatic assays confirmed enzymes (e.g., urease, catalase, citrate and esterase) as drivers of both plastic degradation and heavy metal tolerance in leading isolates. Molecular screening identified the resistance genes pbrA and alkB, while the high prevalence of Class 1 integrons (80% in pbrA-positive isolates) points to a high potential for horizontal gene transfer in these environments. Furthermore, MALDI-TOF MS identified the functional isolates as Bacillus sp. with FTIR verifying the contribution of specific cell-surface functional groups to metal biosorption. These results underscore the promise of native Bacillus strains as promising agents for the development of sustainable, integrated biotechnologies for landfill restoration and complex waste management.

microbiology↗

bioRxiv2025

Supervised machine learning identifies impaired mitochondrial quality control in β cells with development of type 2 diabetes

In type 2 diabetes (T2D), molecular pathways driving {beta} cell failure are difficult to resolve with standard single cell analysis. Here we developed an interpretable, supervised machine learning framework that couples sparse rule-based classification (SnakeClassifier), pathway constrained modelling (BlackSwanClassifier), and {beta} cell mitochondrial fitness stratification (Kolmogorov-Arnold Neural Networks KANN), linking and integrating them into disease mechanisms in single cell RNA sequencing (scRNA-seq) from 52 human donors. SnakeClassifier trained on 50 genes accurately predicted T2D at single cell resolution, outperforming classical ensemble machine learning classifier models, and yielded donor level diabetes scores that correlated with chronic hyperglycemia. The clustering of {beta} cell populations ({beta}1-4) revealed a resilient non-diabetic (ND) {beta}1 subtype characterized by preserved {beta} cell identity genes and lower disease risk, whereas T2D {beta}2-4 subtypes exhibited upregulation of genes involved in cellular and mitochondrial stress and suppression of genes promoting oxidative phosphorylation and insulin secretion. Mitophagy emerged as the dominant program linked to T2D and a mitophagy focused BlackSwanClassifier nominated PINK1, BNIP3, and FUNDC1 as key regulators. PINK1 was enriched in ND {beta}1, decreased with T2D disease score and connected sex stratified mitophagy. We generated a KANN derived mitochondrial fitness index (MFI) integrating mitophagy, mitochondrial proteostasis, biogenesis and oxidative phosphorylation into a single interpretable score (R2 = 0.934 vs module-based mitochondria quality index), which identified mitophagy PINK1, SQSTM1, PRKN and BNIP3 as top contributors to T2D progression. These transparent models unify prediction with T2D disease mechanism and identify the mitophagy receptor PINK1 as a central determinant of {beta} cell metabolic fitness

systems biology↗

bioRxiv2025

Tissue-Specific Co-Expression Patterns of BAF Complexes Provide Regulatory Insights Across Human Tissues with Implications for Endocrine and Non-Endocrine Functions

BRG1/BRM-associated factor (BAF) chromatin remodeling complexes are essential for normal endocrine function and are implicated in various metabolic and developmental disorders. However, the full range of chromatin-based regulatory modules in endocrine development remains unclear. We developed a computational pipeline to analyze bulk RNA-seq data from 54 human tissues and constructed tissue-specific co-expression networks for 30 core BAF complex genes. Weighted gene co-expression network analysis (WGCNA) and Louvain clustering identified gene modules for each tissue, which we compared to 46 curated BAF subcomplex gene sets using Jaccard similarity. In metabolically active non-endocrine tissues (kidney, skeletal muscle, vasculature, fibroblasts), we observed strong co-expression with canonical BAF (cBAF) and polybromo-associated BAF (pBAF) modules. Central nervous system tissues were dominated by neuron-specific BAF (nBAF) modules. Endocrine tissues (e.g., thyroid, adrenal) and gastrointestinal epithelia displayed co-expression profiles resembling smooth muscle-like BAF and pBAF modules, suggesting chromatin programs that integrate hormone secretion with contractile and barrier functions. These patterns show that each tissue exhibits a distinct, non-random combination of BAF subcomplexes, potentially reflecting its functional chromatin state. Our results demonstrate that tissue-specific gene expression profiling can reveal differences in protein complex regulation. The modular deployment of BAF chromatin remodeling complexes appears tailored to the functional demands of each organ. This study lays a foundation for further investigation of epigenetic regulation in endocrine development and disease and provides a framework for identifying tissue-specific chromatin remodeling strategies. Plain Language Summary (optional)The US National Institutes of Health have invested in large-scale measurements of how different human body tissues use their genetic material. This study pilots use of these data to understand better how various genes come together to form nanomachines that in turn regulate the same genetic material.

bioinformatics↗

bioRxiv2025

A Multi-State Structural Genomics Approach Enables Large-Scale, Mechanistic, and Context-Specific Classification of ABCC6 Genetic Variants Implicated in Calcification Diseases

PurposeGenetic variation in ATP Binding Cassette Subfamily C Member 6 (ABCC6) can cause both pseudoxanthoma elasticum (PXE) and generalized arterial calcification of infancy (GACI). Despite both diseases being rare, there are already 930 distinct missense variants in ABCC6 reported, 87% of which are of uncertain clinical significance (VUS). New approaches are needed to interpret and classify these VUS mechanistically. MethodsWe developed 3D protein models of ABCC6 in three functionally relevant conformations to calculate the structural effects of variants and identify 3D mutational hotspots. With this and additional functional information, we categorized variants in a mechanistic ontology based on which critical functions of ABCC6 they impact. We then compared PXE and GACI -associated variants. ResultsWe identified two three-dimensional hotspots of pathogenic variants and six specific functions of ABCC6 which variants impact. From this, we propose a mechanism for pathogenicity for 41% of VUS according to their impacted function, 30 of which could be reclassified as Likely Pathogenic from our non-clinical data. Finally, we found slight differences between PXE and GACI-associated variants. ConclusionThe mechanistic information we present will guide future research to better address calcification disorders and understand genetic variants. Further, our VUS reclassification will improve the diagnosis of ABCC6-driven diseases, shortening diagnostic odysseys. We believe that computational structural genomics approaches will soon take prominence in genomics data interpretation. HighlightsVariant 3D hotspot detection and effect clustering, GACI and PXE Variant Comparison, consistent ability to (re)categorize known pathogenic variants, and population genetics differences.

genetics↗

bioRxiv2025

Dynamic transcription pre-initiation complex assembly governs initiation efficiency

Transcription initiation is a highly regulated process that determines gene expression outcomes1,2, yet the dynamics of initiation and the mechanisms governing efficiency remain poorly understood. Here, we combine endogenous tagging of human RNA polymerase II (Pol II) and TFIID with simultaneous live-cell, multi-color single-molecule imaging to quantitatively map Pol II behavior during transcription initiation and early elongation. Using GRID (Genuine Rate Identification) analysis, we resolved four distinct kinetic populations of chromatin-bound Pol II. The dynamics of Pol II populations reveal that initiation is highly inefficient, with over 94% of Pol II molecules dissociating within tens of seconds. Kinetic partitioning of Pol II dwell times enables quantification of proximal pausing, which is globally sensitive to CDK9 inhibition. Single-cell analysis uncovers substantial heterogeneity in initiation efficiency and pausing across individual cells. Colocalization of Pol II with TFIID is associated with higher initiation efficiency and reduced promoter-proximal pausing compared to global Pol II. Further dissection of Pol II-TFIID assembly pathways reveals that canonical assembly, where TFIID binds first, is linked to inefficient initiation and frequent pausing. In contrast, non-canonical assembly, where Pol II binds first followed by TFIID, supports more efficient initiation with lower pausing. Together, these findings establish that transcription initiation efficiency is shaped by both the kinetic stability of Pol II engagement and the temporal order of pre-initiation complex assembly, providing a new framework for understanding dynamic gene regulation in vivo.

cell biology↗

bioRxiv2025

Uncovering the isoform-resolution kinetic landscape of nonsense-mediated mRNA decay with EZbakR

Cellular RNA levels are a product of synthesis and degradation kinetics, which can differ among transcripts of the same gene. An important cause of isoform-specific decay is the nonsense-mediated mRNA decay (NMD) pathway, which degrades transcripts with premature termination codons (PTCs) and other features. Understanding NMD functions requires strategies to quantify isoform kinetics; however, current approaches remain limited. Methods like nucleotide-recoding RNA-seq (NR-seq) enable insights into RNA kinetics, but existing bioinformatic tools do not provide robust, isoform-specific degradation rate constant estimates. We extend the EZbakR-suite by implementing a strategy to infer isoform-level kinetics from short-read NR-seq data. This approach uncovers unexpected variability in NMD efficiency among transcripts with conserved PTC-containing exons and rapid decay of a subset of mRNAs lacking PTCs. Our findings highlight the effects of competition between NMD and other decay pathways, provide mechanistic insights into established NMD efficiency correlates, and identify transcript features promoting efficient decay.

molecular biology↗

bioRxiv2025

Remodeling of nucleosome by a DNA translocating bacterial restriction-modification enzyme

A eukaryotic cell has specialized ATP-dependent chromatin remodelers, such as SWI/SNF, to unfurl DNA from nucleosome for functional processing. The ATPase that powers the movement of the chromatin remodeler on the DNA (translocation) is evolutionarily related to those powering the translocation of the functionally distinct bacterial restriction-modification (RM) enzymes. The collision of a SWI/SNF chromatin remodeler and a nucleosome, results in sliding/ejection of the constituent histone octamer, while two converging ATP-dependent RM enzymes catalyze DNA cleavage. Here, we investigate if an ATP-dependent Type ISP RM enzyme, an active and directional translocase, can remodel nucleosomes. Our results reveal that in presence of ATP, a Type ISP RM enzyme can displace the octamers from not just mononucleosomes but also two tandem nucleosomes. However, a Type III RM enzyme, which employs a homologous ATPase as a switch to facilitate bidirectional 1D diffusion along the DNA, fails to remodel the nucleosome. This implies that an actively translocating Type ISP RM enzyme generates sufficient force for chromatin remodeling, and may serve as artificial sequence-specific chromatin remodelers.

molecular biology↗

bioRxiv2024

Advancing Variant Phenotyping in Myelodysplastic Syndromes via Computational Genomics of Mitochondrial Enzyme Complexes

Mitochondria are essential cellular organelles that play critical roles in hematological disorders. Recurrent mutations in mitochondrial DNA (mtDNA) have been identified in patients with myelodysplastic syndromes (MDS) and serve as significant prognostic indicators for their outcomes following allogeneic hematopoietic stem-cell transplantation (allo-HCT). However, the biological mechanisms of mtDNA mutations remain unclear. The current study utilizes computational structural genomics to improve our understanding of pathogenic variants in mitochondria-encoded genes. This emerging genomics discipline employs structural models, molecular mechanic calculations, and accelerated molecular dynamic simulations to analyze gene products, focusing on their structures and motions that determine their function. We applied this methodology to perform deep variant phenotyping of entire mitochondria-encoded protein complexes associated with the pathobiology of MDS and their prognosis after HCT. Our results demonstrate that this approach significantly outperforms conventional analytical methods, providing enhanced and more accurate information to support the potential pathogenicity of these variants and better infer their dysfunctional mechanisms. We conclude that the adoption and further expansion of computational structural genomics approaches, as applied to the mitochondrial genome, have the potential to significantly increase our understanding of molecular mechanisms underlying the disease. Our study lays a foundation for translating mitochondrial biology into clinical applications, which is of significant mechanistic and biomedical relevance and should be considered in modern biomedical research.

genomics↗

bioRxiv2023

Beyond Structural Bioinformatics for Genomics with Dynamics Characterization of an Expanded KRAS Mutational Landscape

ABSTRACTCurrent capabilities in genomic sequencing outpace functional interpretations. Our previous work showed that 3D protein structure calculations enhance mechanistic understanding of genetic variation in sequenced tumors and patients with rare diseases. The KRAS GTPase is among the critical genetic factors driving cancer and germline conditions. Because KRAS-altered tumors frequently harbor one of three classic hotspot mutations, nearly all studies have focused on these mutations, leaving significant functional ambiguity across the broader KRAS genomic landscape observed in cancer and non-cancer diseases. Herein, we extend structural bioinformatics with molecular simulations to study an expanded landscape of 86 KRAS mutations. We identify multiple coordinated changes strongly associated with experimentally established KRAS biophysical and biochemical properties. The patterns we observe span hotspot and non-hotspot alterations, which can all dysregulate Switch regions, producing mutation-restricted conformations with different effector binding propensities. We experimentally measured mutation thermostability and identified shared and distinct patterns with simulations. Our results indicate mutation-specific conformations which show potential for future research into how these alterations reverberate into different molecular and cellular functions. The data we present is not predictable using current genomic tools, demonstrating the added functional information derived from molecular simulations for interpreting human genetic variation. Key PointsPlease provide 3 bullet points summarizing the manuscripts contribution to the field (100 characters max per point) 1) We functionally grouped 86 distinct KRAS mutations using MD scores, demonstrating scalability for genomics 2) MD-based groups explain experimental differences and mechanistic information about mutant proteins 3) Demonstrated added functional information from simulations for interpreting human genetic variation

genomics↗

bioRxiv2022

A network of DZF proteins controls alternative splicing regulation and fidelity

Proteins containing DZF (domain associated with zinc fingers) modules play important roles throughout gene expression, from transcription to translation. Derived from nucleotidyltransferases but lacking catalytic residues, DZF domains serve as heterodimerization surfaces between DZF protein pairs. Three DZF proteins are widely expressed in mammalian tissues, ILF2, ILF3, and ZFR, which form mutually exclusive ILF2-ILF3 and ILF2-ZFR heterodimers. Using eCLIP-Seq, we find that ZFR binds across broad intronic regions to regulate the alternative splicing of cassette and mutually exclusive exons. ZFR preferentially binds dsRNA in vitro and is enriched on introns containing conserved dsRNA elements in cells. Many splicing events are similarly altered upon depletion of any of the three DZF proteins; however, we also identify independent and opposing roles for ZFR and ILF3 in alternative splicing regulation. Along with widespread involvement in cassette exon splicing, the DZF proteins control the fidelity and regulation of over a dozen highly validated mutually exclusive splicing events. Our findings indicate that the DZF proteins form a complex regulatory network that leverages dsRNA binding by ILF3 and ZFR to modulate splicing regulation and fidelity.

molecular biology↗

bioRxiv2020

Mechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation

Eukaryotic gene expression is extensively regulated by cellular stress and pathogen infections. We have previously shown that herpes simplex virus 1 (HSV-1) and several cellular stresses cause widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII) in host genes and that the viral immediate early factor ICP27 plays an important role in HSV-1-induced DoTT. Here, we show that HSV-1 infection also leads to widespread changes in alternative polyadenylation (APA) of host mRNAs. In the majority of cases, polyadenylation shifts to upstream poly(A) sites (PAS), including many intronic PAS. Mechanistically, ICP27 contributes to HSV-1-mediated APA regulation. HSV-1- and ICP27-induced activation of intronic PAS is sequence-dependent and does not involve general inhibition of U1 snRNP. HSV1-induced intronic polyadenylation is accompanied by early termination of RNAPII. Finally, HSV-1-induced mRNAs polyadenylated at intronic PAS are exported into the cytoplasm while APA isoforms with extended 3 UTRs are sequestered in the nuclei, both preventing the expression of the full-length gene products. Together with other recent studies, our results suggest that viral infection and cellular stresses induce a multi-faceted host shutoff response that includes DoTT and changes in APA profiles.

molecular biology↗

bioRxiv2019

Activation and inhibition of nonsense-mediated mRNA decay controls the abundance of alternative polyadenylation products

Alternative polyadenylation (APA) produces transcript 3 untranslated regions (3UTRs) with distinct sequences, lengths, stability, and functions. We show here that APA products include a class of cryptic nonsense-mediated mRNA decay (NMD) substrates with extended 3UTRs that gene- or transcript-level analyses of NMD often fail to detect. Transcriptome-wide, the core NMD factor UPF1 preferentially recognizes long 3UTR products of APA, leading to their systematic downregulation. Further, we find that many APA events consistently observed in multiple tumor types are controlled by NMD. Additionally, PTBP1, previously implicated in direct modulation of co-transcriptional polyA site choice, regulates the balance of short and long 3UTR isoforms by inhibiting NMD. Our data suggest that PTBP1 binding near polyA sites can drive production of long 3UTR APA products in the nucleus and/or protect them from decay in the cytoplasm. Together, our findings reveal a widespread role for NMD in shaping the outcomes of APA.

molecular biology↗

bioRxiv2019

Staphylococcus pasteuri isolates (Spvs) from human atherosclerotic plaques mediate virulence, intracellular resistance and transendothelial invasion of macrophages: A mechanistic paradigm for microbial pathogenicity in atherosclerosis

Atherosclerotic cardiovascular disease, a chronic inflammatory condition of multifactorial etiology, is the leading cause of death worldwide. The concept of bacterial persistence has been proposed as one of several contributing factors to this disease. We hypothesized that the infectious agent(s) found at the site of the atheroma may be dormant but perpetuate virulence in response to host defense and other physiological triggers. In this study, we sought to identify the source of persistent infection in human atherosclerotic plaque and define how pathogen virulence and host defenses mediate plaque vulnerability. Whole genome sequencing (WGS) was used to identify bacteria from pure cultures obtained from atherosclerotic tissues of living subjects diagnosed with more than 70% occlusion of the carotid artery undergoing carotid endarterectomy (CE). WGS identified the predominant species as S. pasteuri (Spv) in all CE isolates grown in pure culture except one isolate which was identified as B. licheniformis. All S. pasteuri isolates (Spvs) were found to contain genes for widespread virulence, invasion, and intracellular resistance. As macrophages (M{varphi}s) play a decisive role at all stages of this disease we treated mouse M{varphi}s (RAW 264.7) with Spvs. While all Spvs tested demonstrated their ability to survive phagocytosis, the highly virulent Spvs also activated M{varphi}s and induced trans-endothelial cell migration of these cells which was mediated via the CC chemokine CCL1 and its receptor CCR8. In conclusion, we show that Spvs are found in CE plaques, have the capacity to survive phagocytosis and induce the transmigration of M{varphi}s across an endothelial barrier in a CCL1-CCR8 dependent process. These findings highlight the significance of carotid vessels as a reservoir for S. pasteuri, a pathogen found in products used routinely in human consumption; this may explain how microbial pathogenicity modulates plaque vulnerability in atherosclerosis.

pathology↗