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PubMed2024

A pyruvate transporter in the apicoplast of apicomplexan parasites.

Pyruvate lies at a pivotal node of carbon metabolism in eukaryotes. It is involved in diverse metabolic pathways in multiple organelles, and its interorganelle shuttling is crucial for cell fitness. Many apicomplexan parasites harbor a unique organelle called the apicoplast that houses metabolic pathways like fatty acid and isoprenoid precursor biosyntheses, requiring pyruvate as a substrate. However, how pyruvate is supplied in the apicoplast remains enigmatic. Here, deploying the zoonotic parasite Toxoplasma gondii as a model apicomplexan, we identified two proteins residing in the apicoplast membranes that together constitute a functional apicoplast pyruvate carrier (APC) to mediate the import of cytosolic pyruvate. Depletion of APC results in reduced activities of metabolic pathways in the apicoplast and impaired integrity of this organelle, leading to parasite growth arrest. APC is a pyruvate transporter in diverse apicomplexan parasites, suggesting a common strategy for pyruvate acquisition by the apicoplast in these clinically relevant intracellular pathogens.

Apicoplasts↗

PubMed2026

Structural Basis for Stepwise Substrate Transport and Disease Phenotypic Heterogeneity of the Mitochondrial ADP/ATP Carrier.

The mitochondrial ADP/ATP carrier (AAC) is essential for cellular energy metabolism and responsible for exchanging ADP for ATP across the inner mitochondrial membrane. However, the precise molecular determinants of substrate binding and the mechanisms underlying the phenotypic heterogeneity of AAC-related diseases remain poorly understood. Here, we combined AlphaFold3 predictions, molecular dynamics simulations, and experimental validation to identify and characterize a previously unrecognized ADP-binding site in AAC (site S2), which is distinct from the canonical bottom site (site S1). AlphaFold3 predictions on AAC variants with disrupted site S1 consistently placed ADP at site S2, interacting with residues R188, K92, and K96, a finding that was independently corroborated by our prior MD simulations. Systematic mutagenesis and functional analysis revealed distinct roles for site S2 residues: R188 serves as the primary phosphate-specific anchor; K92 and K96 facilitate initial recruitment and stabilization; and the aromatic ladder (Y187/Y191/F192/Y195) assists the conformational transition of ADP from anti to syn, a critical step enabling downward translocation. Functional characterization demonstrated that mutations in site S2 significantly impaired ADP transport and oxidative phosphorylation. Notably, the spatial distribution of AAC disease mutations correlates with this bipartite architecture: mild PEOA2-associated mutations cluster near site S2 and perturb the local conformation without abolishing binding, whereas lethal mutations cluster near site S1 and disrupt both ADP binding and structural integrity of the m-gate. Our findings provide new mechanistic insights into stepwise substrate transport and potential therapeutic targets for AAC-related diseases.

Mitochondrial ADP, ATP Translocases↗

PubMed2025

Cellodextrin Metabolism and Phosphotransferase System-Catalyzed Uptake in Enterococcus faecalis.

Two PTS transporters involved in the uptake of cellobiose and short cellooligosaccharides were identified in Enterococcus faecalis. Genes coding for the different EII proteins are found in a locus composed of three operonic structures expressing two distinct EIIC (CelC1 and CelC2), two identical EIIB (CelB1 and CelB2) and a unique EIIA (CelA1). The EIIA plays a central role in β-glucoside uptake because it is required not only for β-homodiholosides but also for the diheteroside N-acetylglucosamine-L-asparagine. Depending on their size, cellooligosaccharides are preferably transported either by CelC1 (di-saccharides) or by CelC2 (4 glycosidic residues and more), with tri-saccharides being taken up by both EIIC transporters. Moreover, CelA1B2C2 require CelGHI to be functional, three small proteins, the function of which remains unknown. CelA1B1C1 is the main but not exclusive transporter of cellobiose and chitobiose. It is involved in the transport of other β-glucodisaccharides, such as laminaribiose and sophorose. This PTS can be complemented by other transporters highlighting the existence of a network for β-glucoside uptake. This locus is under the control of CelR, a LevR-like transcription activator.

Enterococcus faecalis↗

PubMed2025

Systematic screen uncovers regulator contributions to chemical cues in Escherichia coli.

In Gram-negative bacteria, the uptake and export of a wide range of molecules, including antibiotics, is facilitated by porins and efflux pumps. Because of their role in regulating small molecule permeability of the outer and inner membrane, these transport machineries are tightly regulated at the transcriptional and post-transcriptional levels. However, regulation of transport by external chemical cues remains poorly understood. Here we investigated transcriptional regulation of three prominent transporter genes in Escherichia coli across 94 defined chemical cues, and simultaneously mapped the contributions of the key regulators MarA, SoxS and Rob to promoter activity. One third of all tested compounds triggered transcriptional changes, the majority of which were previously unknown. Importantly, we exposed main drivers of transport control in E. coli, e.g., bacteriostatic but not bactericidal antibiotics trigger the expression of efflux pumps, and Rob contributes to ~1/3 of all measured transcriptional changes, thereby emerging as a more prominent regulator of transport than previously thought. We showcase the potential of our resource by elucidating the molecular mechanism of antibiotic antagonisms with widely consumed caffeine in E. coli. Altogether, our analysis provides a quantitative overview of how different regulators orchestrate the transcriptional response of major transport determinants to environmental chemical cues.

Escherichia coli↗

PubMed2017

A New Natural Product Analog of Blasticidin S Reveals Cellular Uptake Facilitated by the NorA Multidrug Transporter.

The permeation of antibiotics through bacterial membranes to their target site is a crucial determinant of drug activity but in many cases remains poorly understood. During screening efforts to discover new broad-spectrum antibiotic compounds from marine sponge samples, we identified a new analog of the peptidyl nucleoside antibiotic blasticidin S that exhibited up to 16-fold-improved potency against a range of laboratory and clinical bacterial strains which we named P10. Whole-genome sequencing of laboratory-evolved strains of Staphylococcus aureus resistant to blasticidin S and P10, combined with genome-wide assessment of the fitness of barcoded Escherichia coli knockout strains in the presence of the antibiotics, revealed that restriction of cellular access was a key feature in the development of resistance to this class of drug. In particular, the gene encoding the well-characterized multidrug efflux pump NorA was found to be mutated in 69% of all S. aureus isolates resistant to blasticidin S or P10. Unexpectedly, resistance was associated with inactivation of norA, suggesting that the NorA transporter facilitates cellular entry of peptidyl nucleosides in addition to its known role in the efflux of diverse compounds, including fluoroquinolone antibiotics.

Bacterial Proteins↗

PubMed2004

Function-informed transcriptome analysis of Drosophila renal tubule.

BACKGROUND: Comprehensive, tissue-specific, microarray analysis is a potent tool for the identification of tightly defined expression patterns that might be missed in whole-organism scans. We applied such an analysis to Drosophila melanogaster Malpighian (renal) tubule, a defined differentiated tissue. RESULTS: The transcriptome of the D. melanogaster Malpighian tubule is highly reproducible and significantly different from that obtained from whole-organism arrays. More than 200 genes are more than 10-fold enriched and over 1,000 are significantly enriched. Of the top 200 genes, only 18 have previously been named, and only 45% have even estimates of function. In addition, 30 transcription factors, not previously implicated in tubule development, are shown to be enriched in adult tubule, and their expression patterns respect precisely the domains and cell types previously identified by enhancer trapping. Of Drosophila genes with close human disease homologs, 50 are enriched threefold or more, and eight enriched 10-fold or more, in tubule. Intriguingly, several of these diseases have human renal phenotypes, implying close conservation of renal function across 400 million years of divergent evolution. CONCLUSIONS: From those genes that are identifiable, a radically new view of the function of the tubule, emphasizing solute transport rather than fluid secretion, can be obtained. The results illustrate the phenotype gap: historically, the effort expended on a model organism has tended to concentrate on a relatively small set of processes, rather than on the spread of genes in the genome.

Animals↗

PubMed2026

Exploring the role of gut microbiota in coronary atherosclerosis through lipoprotein-mediated cholesterol transport and distribution: A Mendelian randomization analysis.

We employed Mendelian randomization (MR) to explore causal relationships between gut microbiota (GM), coronary atherosclerotic heart disease (CAHD), and potential metabolic mediators. We utilized summary statistics from genome-wide association studies (GWAS), encompassing data on 473 GM traits from comprehensive microbiome GWAS, 61 lipoprotein-mediated cholesterol transport and distribution data from large-scale metabolic biomarker studies, and coronary atherosclerosis (CA) data from the GWAS catalog (study accession GCST90043957) involving 456,348 European participants. Bidirectional MR analyses were conducted to investigate the causal relationships between GM and CA. Two-sample Mendelian randomization analyses were performed to identify potential mediating metabolites and quantify the mediation proportion. Ultimately, the GM GCA-900066755, identified through MR as having a potential causal relationship, was selected to investigate its potential effects on CA by influencing cholesterol transport and distribution. Our results indicated that GCA-900066755 was positively associated with an increased risk of CA (odds ratio = 1.156). CA did not significantly affect the levels of GCA-900066755 (odds ratio = 1.009). GCA-900066755 was negatively correlated with total cholesterol levels in medium high-density lipoprotein, which reduced CA risk, and was positively correlated with total cholesterol levels in low-density lipoprotein (LDL), large LDL, medium LDL, and small LDL, which were positively associated with CA. Mediation analysis showed 7 data points mediating the association between GCA-900066755 and CA. Our MR study supports a causal relationship between specific GM groups and the risk of CAHD, highlighting that cholesterol traits are not merely outcomes associated with the relationship between GM and CAHD, but are important mediating factors. Understanding the biological mechanisms of these traits can provide a concrete foundation for future targeted interventions.

Mendelian Randomization Analysis↗

PubMed2026

A maize GT14 family glycosyltransferase affects cell wall composition and carbohydrate export from source leaves.

Sucrose translocation from photosynthetic leaves to distant parts of a plant, such as seeds and roots, is a critical aspect of plant growth and development and a major determinant of crop yield. To identify genes contributing to this process in maize (Zea mays), we isolated four allelic mutants, carbohydrate partitioning defective7, 48, 49 (cpd7, cpd48, cpd49) and a UniformMu insertion (mu1049954), all of which exhibited reduced growth and fertility and hyperaccumulation of starch and soluble sugars in mature leaves. Consistent with carbohydrate accumulation, cpd7 mutants exhibited reduced sucrose export from mature leaves. Cpd7 encodes a Golgi-resident glucuronosyltransferase belonging to the Glycosyltransferase14 (GT14) family, which is involved in decoration of type II arabinogalactan proteins. No previously described GT14 mutants exhibit reduced sucrose transport or carbohydrate partitioning defects. Additionally, we show that mature leaves of cpd7 mutants have reduced cellulose content and an altered cell wall composition. Further, cpd7 mutants exhibit ectopic phloem lignification likely as a compensatory mechanism for reduced cell wall integrity. Collectively, our data suggest that Cpd7 functions to facilitate cell wall development in the phloem, which is required for efficient sucrose export from mature maize leaves.

Zea mays↗

PubMed2025

Sphingobium yanoikuyae 41R9 Enhances Nitrogen Uptake by Modulating Transporter Genes and Root Development in Rapeseed.

Plant growth-promoting rhizobacteria (PGPR) are widely recognized for enhancing the absorption of mineral nutrients by crops. While Sphingobium species have been reported as PGPRs, their capacity to improve nitrogen use efficiency (NUE) and the underlying regulatory mechanisms are not yet fully understood. Here, a strain 41R9, isolated from the rhizosphere of N-deficient rapeseed, was found to significantly enhance the growth performance of rapeseed under both low and normal N conditions. Genomic analysis revealed that strain 41R9 was closely related to Sphingobium yanoikuyae. 15N isotope tracer experiments confirmed that inoculation with strain 41R9 significantly boosted N uptake and translocation in rapeseed roots. Transcriptome profiling demonstrated that strain 41R9 directly upregulated N transporter genes (NRT2.5 and SLAH1/3), facilitating efficient N acquisition. Furthermore, strain 41R9 maintained jasmonic acid (JA) homoeostasis via JAZ-mediated negative feedback, balancing defense responses and root development, thereby improving the plant's N acquisition capacity in the roots. Metabolomic and in vitro assays further demonstrated that strain 41R9 displayed strong chemotaxis towards kaempferol, a N-deficiency-induced root exudate, suggesting kaempferol might as a chemical effector for S. yanoikuyae recruitment. These findings advance our understanding of PGPR-driven mechanisms in enhancing crop NUE and highlight the potential of harnessing PGPRs for sustainable agriculture.

Plant Roots↗

PubMed2025

The adjacent ATP-binding protein-encoding genes of the Enterococcus faecalis phosphate-specific transport (pst) locus have non-overlapping cellular functions.

UNLABELLED: The widely conserved pst-phoU operon encodes a low-velocity, high-affinity, ATP-dependent importer for inorganic phosphate (Pi). The pstB gene encodes the ATPase that powers the import of Pi into the cell. In some Firmicutes, including the gastrointestinal commensal and opportunistic pathogen Enterococcus faecalis, the pst-phoU locus contains adjacent pstB genes. In this work, we compared the functionality of E. faecalis pstB1 and pstB2. E. faecalis pstB1 and pstB2 share sequence similarities with verified PstB ATPases from Escherichia coli and Streptococcus pneumoniae and only share ~60% amino acid identity with each other. Deletion of pstB1 was associated with a growth defect in low Pi-containing chemically defined medium (CDM), reduced Pi uptake, and a moderate increase in alkaline phosphatase (AP) activity. Deletion of pstB2 fully inhibited growth in CDM regardless of inorganic phosphorus source but did not hinder growth in rich, undefined medium. The ΔpstB2 mutant also exhibited a significant increase in AP activity that was associated with extracellular Pi accumulation. Overexpression of pstB2 in the pstB1 mutant was sufficient to restore growth in low-Pi CDM, Pi uptake, and AP activity, but this was not recapitulated with overexpression of pstB1 in the ΔpstB2 mutant. Deletion of either pstB paralog increased expression of the tandem paralog, and overexpression of pstB2 in ΔpstB2 reduced pstB1 expression. These results suggest that the E. faecalis pstB2-encoded ATPase is required for Pi import, while the pstB1-encoded ATPase has an accessory role in Pi import that can be duplicated by the presence of excess PstB2. IMPORTANCE: Phosphate is critical for all microbial life. In many bacteria, inorganic phosphate (Pi) is imported by the high-affinity, low-velocity Pst-PhoU system. The pstB gene encodes the ATPase that powers Pi import. The pst-phoU operon in many Firmicutes, including the human commensal and opportunistic pathogen Enterococcus faecalis, contains adjacent pstB genes, pstB1 and pstB2. No studies on the relative biological contributions of tandem pstB paralogs in any microbe have been published. This genetic study indicates that E. faecalis pstB1 and pstB2 do not have equivalent functions. The pstB2 gene encodes an ATPase that is required for Pi import, while the ATPase encoded by pstB1 has an accessory role in Pi import that can be duplicated by the presence of excess PstB2.

Enterococcus faecalis↗

PubMed2025

Pulcherriminic acid biosynthesis and transport: insights from a heterologous system in Saccharomyces cerevisiae.

Pulcherriminic acid is an iron chelator produced by some Kluyveromyces and Metschnikowia yeasts. Its biosynthesis is encoded by the four-gene PUL cluster, where PUL1 and PUL2 are the biosynthetic enzymes, PUL3 mediates the uptake of iron-bound pulcherrimin, and PUL4 is a putative regulator. Pulcherriminic acid holds antifungal potential, as the growth of organisms unable to uptake pulcherrimin is inhibited by deficit of essential iron. Thus, a heterologous production system to further characterize and optimize its biosynthesis would be valuable. Using our in-house yeast collection and genomes available in databases, we cloned PUL1 and PUL2 genes from Kluyveromyces lactis and one of our wild Metschnikowia isolates and built an effective production system in Saccharomyces cerevisiae able to inhibit pathogenic growth. In this context, the K. lactis genes yielded faster pulcherriminic acid production than those from the Metschnikowia isolate and a combinatorial approach showed PUL1 to be the production bottleneck. We further showed that Pul3 is an importer of pulcherrimin, but also mediates the export of pulcherriminic acid and that the growth of pathogens such as Candidozyma auris and organisms encoding PUL3 in their genome, previously called "cheaters," is inhibited by pulcherriminic acid, highlighting its potential as an antimicrobial agent.

Saccharomyces cerevisiae↗

PubMed2026

Bacterial extracellular vesicles exhibit distinct functional potential across biogeographic provinces of the South Pacific Ocean.

Bacterial extracellular vesicles (BEVs) are nanoscale membranous structures released by diverse types of bacteria, and are capable of transporting and delivering biological compounds between cells. Experimental investigation of BEVs in laboratory model systems indicates that these nanoparticles may play a number of roles in the ecophysiology of marine bacterial communities, but their functional potential in the environment remains unclear. Here we describe the proteomic composition of BEV populations over more than 5000 nautical miles of surface waters in the South Pacific, linking BEV cargoes to the bacterial communities producing them. The presence of marine BEVs was consistently observed across a range of biogeochemical conditions, with an overall abundance comparable to that of bacterial cells (up to 108 BEVs L-1). The protein cargo of marine BEVs, however, differed significantly among ocean regions. The BEV populations were enriched in carbohydrate transporters under phytoplankton bloom conditions, and contained iron uptake-related proteins in nutrient-limited waters. These data suggest that BEVs could enable cells to perform key extracellular functions in the marine environment. Our observations highlight the ubiquity of marine BEVs and biogeographic patterns in their ecological potential across oceanic scales.

Extracellular Vesicles↗

PubMed2026

Targeting ncRNA control networks with engineered exosomes to overcome therapy resistance in thyroid cancer.

Papillary thyroid cancer (PTC) is the most prevalent endocrine malignancy, accounting for over 90% of thyroid cancers. While differentiated thyroid cancers (DTCs) typically have favorable outcomes, a significant subset progresses to radioactive iodine-refractory (RAIR) disease, characterized by impaired iodine uptake and a 10-year survival rate below 10%. Genetic alterations and dysregulated signaling pathways underlie this transition. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs), play critical regulatory roles in tumor biology and may be transported via exosomes, facilitating intercellular communication and contributing to RAIR-PTC. This systematic review, conducted according to PRISMA 2020 guidelines, evaluated the role of exosomal ncRNAs in RAIR-PTC. A comprehensive search of PubMed, PubMed Central, and Google Scholar identified studies published within the past 15 years in English. Following stringent quality appraisal, studies with a non-bias score above 40% were included. Of 961 identified publications, 96 high-quality studies met inclusion criteria. Evidence indicates that therapy resistance in RAIR-PTC is driven by convergent ncRNA regulatory networks that suppress sodium-iodide symporter (NIS) expression and activate oncogenic pathways, most notably MAPK, PI3K/AKT/mTOR, and Wnt/β-catenin signaling. Multiple ncRNAs converge on key regulatory nodes, forming redundant circuits that sustain dedifferentiation, metabolic adaptation, and impaired iodide transport. Several consistently dysregulated ncRNAs directly or indirectly regulate NIS expression and trafficking, highlighting actionable targets. Exosomes emerge as biologically compatible, programmable delivery vehicles capable of transporting therapeutic ncRNA payloads independent of endogenous packaging mechanisms. These findings support a precision therapeutic paradigm in which engineered exosomes reprogram ncRNA networks to restore iodine-handling pathways and overcome therapy resistance in RAIR-PTC.

Humans↗

PubMed2026

Disentangling Sex Differences in Sulfonylurea Drug Response With Genome-Wide Association Studies in Individuals With Type 2 Diabetes.

Sulfonylureas are a cornerstone of type 2 diabetes therapy despite interindividual variability in response. Despite well-documented sex-based differences, pharmacogenomic and genome-wide association studies (GWAS) have largely overlooked sex as a biological variable. We conducted the first sex-stratified GWAS of hemoglobin A1c (HbA1c) response to sulfonylureas in Action to Control Cardiovascular Risk in Diabetes (ACCORD) clinical trial participants (N = 871). Variants meeting genome-wide (P < 5.0 × 10-8) and suggestive (P < 5.0 × 10-6) significance were assessed for replication in the Pharmacogenomics of Metformin (PMET1) cohort. Replicated variants were further analyzed in the Study to Understand the Genetics of the Acute Response to Metformin and Glipizide in Humans (SUGAR-MGH) cohort to assess acute insulin and glucose responses to a single glipizide dose. Genome-wide significant loci with sex-specific effects were identified: KAZN, KIF2B, SLC39A10, and SPINK5 (combined-sex); CRACR2A, KCNK2, and TENM2 (male-only); and NACPH2 (female-only). Two suggestive variants in the TMEM64/NECAB1 locus, associated with reduced HbA1c response to sulfonylureas in the male-only ACCORD analysis, were directly replicated in the PMET1 male-only cohort. In SUGAR-MGH, one replicated variant (rs6471250-C) was significantly associated with reduced peak insulin in males (P = 0.035) but not females (P = 0.40), demonstrating sex-specific functional effects. This study identified statistically supported and biologically plausible loci with prior evidence linking nearby genes to pathways relevant to sulfonylurea action, including insulin secretion, insulin regulation/sensitivity, calcium signaling, potassium-channel biology, and glucose transport. The findings highlight sex-specific differences in sulfonylurea response, providing mechanistic insights and underscoring the importance of sex-specific precision medicine. Identification of genetic variants influencing sex-specific response could inform dosing to optimize sulfonylureas.

Humans↗

PubMed2025

Investigating milk-derived extracellular vesicles as mediators of maternal stress and environmental intervention.

Parental communication signals are transmitted through nursing and critically shape neurodevelopmental trajectories. Mirroring some well characterized effects of gestational challenges in rodents, maternal immune activation (MIA) during the lactational period disrupts maternal physiology, decreases lipid content, and is associated with adverse neurobehavioral outcomes in offspring. This occurs without MIA significantly affecting maternal care. While gestational MIA models are responsive to environmental interventions, which beneficially alter maternal milk composition and associated offspring outcomes, the bioactive mediators in milk underlying resilience remain poorly understood. Milk-derived extracellular vesicles (MEVs) transport and deposit biologically active cargo, including microRNAs (miRNAs) that induce post-translational regulation of candidate mRNA in the nursing offspring's tissues and cells. Using a rat model, we show that lactational MIA alters MEV-miRNA cargo and the expression of hippocampal miRNAs in offspring. Several miRNAs in MEVs were also found in the hippocampus of matching offspring. Remarkably, the miRNA changes in MEVs and the neonatal hippocampus were rescued when dams were raised in an enriched environment, suggesting environmental enrichment protected from the effects of MIA. This was supported by the behavioral phenotype. RNA-seq of adult offspring hippocampus showed long-term transcriptional changes associated with the gene targets of early-life regulated miRNAs. Our results position MEV-miRNA as dynamic programming signals by which maternal experience is communicated to offspring, encoding both stress-induced and protective cues that influence development. This suggests that breastfeeding interventions can regulate the genetic cargo of the milk, programming the life of developing infants.

Journal Article↗

PubMed2026

Cu(II/I)-Pyridinophane Complexes: O2 Reactivity and 64Cu PET Imaging Studies.

The redox versatility of copper between the Cu(I) and Cu(II) oxidation states is central to its function in a variety of biological processes, including electron transfer, oxygen transport, and redox catalysis by metalloenzymes. Motivated by these biological paradigms, we report the design and development of a new series of chelators based on the 2-aza[3,2](2,6)pyridinophane (RN3) ligands (RN3, R = H, Me, 2-methylpyridyl, and 2-methylpicolinate). These ligands are designed to replicate key features of metalloenzyme active sites and to modulate the copper coordination environment. The new RN3 ligands have been fully characterized by NMR spectroscopy, high-resolution mass spectrometry, and UV-vis spectrophotometric titrations. The Cu(I) and Cu(II) complexes supported by these ligands were synthesized and characterized structurally and spectroscopically to investigate the effects of ligand denticity, variation in donor atoms, and chelate ring size on coordination geometry, bond parameters, and redox behavior. Special attention is given to the reactivity of Cu(I) complexes toward O2, offering insights into pathways of O2 activation and reduction. The RN3 ligands also demonstrate promising stability and binding affinity for both Cu(II) and Cu(I) ions, underscoring their potential for 64Cu-based positron emission tomography (PET) imaging applications.

Journal Article↗

PubMed2026

Urban stormwater infrastructure as a microplastic superhighway: a critical review of transport dynamics, modelling, and mitigation across pavements and drainage networks.

This review examines the transport, fate, modelling, and mitigation of Microplastics (MPs) in urban stormwater infrastructure, with emphasis on pavements, runoff pathways, micro-drainage, and macro-drainage systems. Following a systematic review approach, more than 1000 records were screened and approximately 50 core studies were retained when they addressed urban stormwater or drainage-related MP transport with adequate methodological reporting; marine-only studies and biological-effect studies without direct relevance to transport processes were excluded. The evidence shows that stormwater systems function not merely as passive conduits but as dynamic reactive transport systems with temporary storage, where particle mobilisation, sedimentation, resuspension, and temporary retention regulate MP export. Road surfaces, especially high-traffic areas, are major reservoirs of tyre wear, road-marking, atmospheric, and litter-derived particles that are rapidly mobilised during rainfall. Conventional grab sampling may underestimate MP loads, which in some cases exceed treated wastewater effluent loads by up to six-fold. Drainage structures such as manholes can immobilise up to 17.3% of near-neutrally buoyant particles, while biofouling and aggregation may shift buoyant polymers from wash-load to bedload. Mitigation systems, including permeable pavements, bioretention, wetlands, and technical inserts, can achieve high removal of coarse MPs, but performance declines for fine particles below 100 µm. The review highlights the need for standardised flow-proportional sampling, physically informed modelling, and treatment-train strategies targeting both surface sources and in-network storage.

Microplastics↗

PubMed2016

A synergistic approach to the design, fabrication and evaluation of 3D printed micro and nano featured scaffolds for vascularized bone tissue repair.

3D bioprinting has begun to show great promise in advancing the development of functional tissue/organ replacements. However, to realize the true potential of 3D bioprinted tissues for clinical use requires the fabrication of an interconnected and effective vascular network. Solving this challenge is critical, as human tissue relies on an adequate network of blood vessels to transport oxygen, nutrients, other chemicals, biological factors and waste, in and out of the tissue. Here, we have successfully designed and printed a series of novel 3D bone scaffolds with both bone formation supporting structures and highly interconnected 3D microvascular mimicking channels, for efficient and enhanced osteogenic bone regeneration as well as vascular cell growth. Using a chemical functionalization process, we have conjugated our samples with nano hydroxyapatite (nHA), for the creation of novel micro and nano featured devices for vascularized bone growth. We evaluated our scaffolds with mechanical testing, hydrodynamic measurements and in vitro human mesenchymal stem cell (hMSC) adhesion (4 h), proliferation (1, 3 and 5 d) and osteogenic differentiation (1, 2 and 3 weeks). These tests confirmed bone-like physical properties and vascular-like flow profiles, as well as demonstrated enhanced hMSC adhesion, proliferation and osteogenic differentiation. Additional in vitro experiments with human umbilical vein endothelial cells also demonstrated improved vascular cell growth, migration and organization on micro-nano featured scaffolds.

Bone Regeneration↗