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Ching, C.

Publications and source records attributed to Ching, C..

At least 19 recordsLinked to original sources

eIF3 interactions with miRNAs involved in translational control of early T cell activation

Early T cell activation induces extensive remodeling of the cellular transcriptome and proteome. We previously showed using a transcriptome-wide crosslinking approach that human translation initiation factor eIF3 directly interacts with a select set of immune-related mRNAs shortly after T cell activation. We also found that eIF3 binding to the 3'-untranslated regions (3'-UTRs) of the TCRA and TCRB mRNAs encoding the T cell receptor alpha and beta subunits dynamically regulates a burst in their translation. MicroRNAs (miRNAs) add an additional layer of regulation by fine-tuning both mRNA and protein expression. Although miRNA expression is dynamically regulated during T cell activation, how miRNAs interact with core regulatory pathways in primary T cells remains poorly understood. Here, we reexamined the eIF3-RNA crosslinking experiments in Jurkat cells and probed eIF3 function to investigate miRNA-mediated translational regulation during T cell activation. We found that eIF3 interacts with multiple mature miRNAs in activated Jurkat cells, including members of the miR-17[~]92 cluster. These interactions also occur in primary T cells, as shown by RNA immunoprecipitation followed by qPCR (RIP-qPCR). Knocking out the miR-17[~]92 cluster led to a delay in ILR2A (CD25) cell surface expression in Jurkat cells and reduced activation-associated cell size increase in primary T cells during early T cell activation. In parallel, we used mass spectrometry to identify eIF3-interacting factors in activated primary T cells, and surprisingly found no evidence of Argonaute binding. Together, these findings provide evidence that eIF3-miRNA interactions may play an unappreciated role in translational control during early T cell activation.

Molecular Biology↗

Virus-like particles enable targeted gene engineering and pooled CRISPR screening in primary human myeloid cells

Primary human myeloid cells are promising candidates for immunotherapy, yet efficient and scalable technologies for genetic engineering and screening in these cells are limited. Here we present a virus-like particle (VLP)-based toolkit that delivers diverse CRISPR genome editing modalities to human monocytes, macrophages, and dendritic cells with high efficiency while preserving viability and innate immune responsiveness. VLP-mediated delivery of ribonucleoprotein payloads supports gene knockout, base editing and epigenetic silencing, and enables site-specific integration of large DNA sequences when combined with AAV donors for homology-directed repair. Leveraging sgRNA delivery via VPX-lentivirus combined with Cas9 protein delivery via engineered virus-like particle (eVLP) treatment ("SLICeVLP"), we performed the first pooled loss-of-function screens in human macrophages. We uncovered regulators of TNF production and CD80 expression in human macrophages, converging on TNFAIP3 as a central regulator of inflammatory polarization. TNFAIP3 ablation promoted a pro-inflammatory cell state that is resistant to suppressive polarization, and augmented cytotoxicity of engineered HER2 CAR-macrophages. Taken together, this technology platform enables unbiased discovery and characterization of functional gene targets in primary human myeloid cells.

immunology↗

Reduction of Aβ25-35-Induced Cognitive Impairments in C57BL/6 Mice Through Focused Ultrasound Thermal-Cycling Stimulation

Hyperthermia (HT) is recognized across various medical disciplines for its capacity to modulate specific protein expressions. In efforts to improve Alzheimers disease (AD), HT has the potential to regulate heat shock proteins (HSPs) and antioxidant enzymes, which helps decrease the aberrant accumulation of {beta}-amyloid (A{beta}) protein and oxidative stress. Nonetheless, the precise delivery of mild hyperthermia to the brain remains a significant challenge. To apply mild hyperthermia targeted to the brain and evaluate its impact on cognitive improvement, this study used focused ultrasound (FUS) to administer localized mild hyperthermia to the brains of AD mouse induced by intracerebroventricular (i.c.v.) injection of A{beta}25-35. For considerations of safety and therapeutic efficacy, a thermal cycling-hyperthermia (TC-HT) protocol was adapted into a focused ultrasound-mediated thermal cycling stimulation (FUS-TCS), which was compared with the continuous focused ultrasound-mediated hyperthermia stimulation (FUS-HTS). The findings revealed that the FUS-TCS treatment group exhibited a significant improvement in cognitive performance, as evidenced by enhanced outcomes in the Y-maze and novel object recognition (NOR) tests. Furthermore, this group demonstrated increased expression of A{beta}-degrading enzymes and antioxidant proteins, including heat shock protein 70 (HSP70), neprilysin (NEP), insulin degrading enzyme (IDE), sirtuin 1 (SIRT1), and superoxide dismutase 2 (SOD2). These results suggest that localized mild hyperthermia targeting the brain using FUS-TCS treatment represents a promising strategy for ameliorating cognitive deficits associated with AD.

neuroscience↗

Base-editing a single missense mutation in A20 enhances CAR-T cell efficacy

T cell exhaustion limits the efficacy of cancer immunotherapies. Here, we performed genome-wide loss-of-function screening in repetitively stimulated human T cells and identified the mulitfunctional ubiquitin-modifying protein A20/TNFAIP3 as a major negative regulator of exhausted T cell persistence. Protein large language modeling, deep base-editing mutagenesis, and studies in immunocompetent mice with domain-specific inactivating mutations revealed A20s non-enzymatic M1 ubiquitin-binding zinc finger 7 (A20ZF7) motif as critical to suppression of anti-tumor immunity. A20ZF7-deficient CD8+ tumor-infiltrating lymphocytes (TILs) resisted terminal exhaustion and circumvented an unappreciated mechanism restraining perforin degranulation in terminally exhausted cells. Human chimeric antigen receptor (CAR)-T cells engineered via base-editing to inactivate A20ZF7 via a single missense mutation also resisted exhaustion, secreted more perforin and robustly suppressed cancer in vivo. These studies pinpoint A20ZF7 as a novel T cell checkpoint and reveal precision base-editing of missense mutations as an effective approach to enhance CAR-T cell therapy.

immunology↗

Thermal cycling stimulation via nasal inhalation attenuates Aβ25-35-induced cognitive deficits in C57BL/6 mice

Alzheimers disease (AD) continues to pose a significant public health challenge, with current treatments demonstrating limited effectiveness, partly due to the difficulty of delivering therapeutics across the blood-brain barrier (BBB). The nose-to-brain (N-2-B) pathway offers a promising alternative, enabling pharmacological agents to circumvent the BBB. However, to date, no drugs have been successfully implemented in clinical settings for the treatment of AD via this route, underscoring the necessity for additional research in this area. Mild stress is thought to activate intrinsic protective mechanisms against neurodegeneration, but traditional methods of inducing stress often lack both specificity and practicality. To address this limitation, we propose the inhalation of mildly heated air as a form of thermal stimulation, which utilizes the N-2-B pathway to induce mild stress and stimulate cerebral activity. This study employs the method of thermal cycling-hyperthermia (TC-HT) technique [Chao C.Y. et al., U.S. patent 11753634, 2023 & Chao C.Y. et al., U.S. patent Appl. No. 18/864192, 2024] into a new treatment, adapted as thermal cycling-stimulation via nasal inhalation (TCSNI), which provides cyclic stimulation to maintain pathway activity while minimizing thermal injury. In this study, we assessed the health and olfactory effects of TCSNI in C57BL/6 mice and found no adverse effects. In experimental groups administered with {beta}-amyloid (A{beta}), TCSNI treatment resulted in significant enhancements in cognitive performance as evidenced by Y-maze and novel object recognition (NOR) assessments, suggesting an improvement in cognitive function. Protein analyses conducted on the hippocampus of the mice indicated a reduction in A{beta} accumulation, alongside increased expression of heat shock protein 70 (HSP70) and insulin-degrading enzyme (IDE) expression, as well as elevated levels of phosphorylated Akt (p-Akt). These results suggest that N-2-B-delivered TCSNI effectively modulates protein expression and enhances cognitive function, highlighting its potential for further exploration in AD treatment.

neuroscience↗

Cellular behavior analysis from live-cell imaging of TCR T cell-cancer cell interactions

T cell therapies, such as chimeric antigen receptor (CAR) T cells and T cell receptor (TCR) T cells, are a growing class of anti-cancer treatments. However, expansion to novel indications and beyond last-line treatment requires engineering cells dynamic population behaviors. Here we develop the tools for cellular behavior analysis of T cells from live-cell imaging, a common and inexpensive experimental setup used to evaluate engineered T cells. We first develop a state-of-the-art segmentation and tracking pipeline, Caliban, based on human-in-the-loop deep learning. We then build the Occident pipeline to collect a catalog of phenotypes that characterize cell populations, morphology, movement, and interactions in co-cultures of modified T cells and antigen-presenting tumor cells. We use Caliban and Occident to interrogate how interactions between T cells and cancer cells differ when beneficial knock-outs of RASA2 and CUL5 are introduced into TCR T cells. We apply spatiotemporal models to quantify T cell recruitment and proliferation after interactions with cancer cells. We discover that, compared to a safe harbor knockout control, RASA2 knockout T cells have longer interaction times with cancer cells leading to greater T cell activation and killing efficacy, while CUL5 knockout T cells have increased proliferation rates leading to greater numbers of T cells for hunting. Together, segmentation and tracking from Caliban and phenotype quantification from Occident enable cellular behavior analysis to better engineer T cell therapies for improved cancer treatment.

cell biology↗

Characterization of antibiotic resistance development of E. coli in synthetic and real wastewater

Antimicrobial resistance (AMR) is a major threat to global health and resistant bacterial populations have been observed to develop and spread in and around wastewater. However, in vitro studies on AMR development are typically conducted in ideal media conditions which can differ in composition and nutrient density from wastewater. In this study, we compare the growth and AMR development of E. coli in standard LB broth to a synthetic wastewater recipe and autoclaved wastewater samples from the Massachusetts Water Resources Authority (MWRA). We found that synthetic wastewater and real wastewater samples both supported less bacterial growth compared to LB. Additionally, bacteria grown in synthetic wastewater and real wastewater samples had differing susceptibility to antibiotic pressure from Doxycycline, Ciprofloxacin, and Streptomycin. However, AMR development over time during continuous passaging under subinhibitory antibiotic pressure was similar in fold change across all media types. Thus, we find that while LB can act as a proxy for wastewater for AMR studies in E. coli, synthetic wastewater is a more accurate predictor of both E.coli growth and antibiotic resistance development. Moreover, we also show that antibiotic resistance can develop in real wastewater samples and components within wastewater likely have synergistic and antagonistic interactions with antibiotics. ImportanceAntimicrobial resistance (AMR) ranks among the leading global threats to public health and development. In 2019, bacterial AMR was estimated to have directly caused 1.27 million deaths worldwide and contributed to 4.95 million deaths overall (Murray, C. J., et al., (2022). Global burden of bacterial antimicrobial resistance in 2019: a systematic analysis. The Lancet, 399(10325), 629-655.). With estimations of AMR only getting worse, it is imperative that we understand the complex dimensionalities that drive the genesis of antimicrobial resistance to where it begins-the environment. The paper investigates bacterial growth and AMR in real wastewater samples and highlights the importance of using a media that closely mimics real wastewater in AMR studies, compared to standard lab media like LB broth. This is crucial for understanding how E. coli and other bacteria develop AMR in environments similar to actual wastewater, which can inform more effective strategies to combat AMR in natural and engineered settings.

microbiology↗

Multiple transcription factors regulate the expression of genes for error prone DNA polymerases in Acinetobacter baumannii

Acinetobacter baumannii is an opportunistic pathogen causing several infections that are increasingly diSicult to treat due to its ability to rapidly gain antibiotic resistances. These resistances can arise due to mutations during the DNA damage response (DDR), through the activity of error-prone DNA polymerases, such as DNA polymerase V (DNA Pol V). Currently, the DDR in A. baumannii is not well understood and the regulation of genes encoding multiple copies of DNA Pol V is not fully characterized. Through genome wide mutagenesis, we have identified a novel TetR-like family regulator of genes that encode DNA Pol V, which we have named Error-prone polymerase regulator, EppR. We have found that EppR represses the expression of the genes encoding DNA Pol V and itself through direct binding to a conserved EppR motif in their promoters. Lastly, we show that EppR also regulates UmuDAb, previously identified as a regulator of genes encoding DNA Pol V. These two gene products are functionally required to ensure regulation of expression of genes encoding DNA Pol Vs and umuDAb. With these results, we propose a co-repressor model for the regulation of genes encoding DNA Pol V and umuDAb. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=155 SRC="FIGDIR/small/615892v1_ufig1.gif" ALT="Figure 1"> View larger version (17K): org.highwire.dtl.DTLVardef@502a49org.highwire.dtl.DTLVardef@10844bcorg.highwire.dtl.DTLVardef@1d8be41org.highwire.dtl.DTLVardef@b2a68e_HPS_FORMAT_FIGEXP M_FIG Graphical Abstract C_FIG

microbiology↗

Microplastics as a novel substrate for antimicrobial resistance: Effects of concentration, composition, and size on E. coli multidrug resistance

Microplastics (MPs) have emerged as a significant environmental pollutant with profound implications for public health, particularly as substrates to facilitate bacterial antimicrobial resistance (AMR). Recently, studies have shown that MPs may accommodate microbial communities, chemical contaminants and genetic material containing AMR genes. This study investigated the effects of MP concentration, composition, and size on the development of multidrug resistance in Escherichia coli. Specifically, we exposed E. coli to varying concentrations of different MP types, including polyethylene (PE), polystyrene (PS), and polypropylene (PP), across a range of sizes (3-10 {micro}m, 10-50 {micro}m, and 500 {micro}m). Results indicated a direct correlation between MP presence and elevated multidrug-resistant (MDR) in E. coli. Notably, MPs exhibited a higher propensity for facilitating resistance than control substrates such as glass, likely due to their hydrophobicity, greater adsorption capacities, and surface chemistries. Furthermore, we observed that co-culture with MPs resulted in biofilm formation. Notably, we found that the bacteria from passaged MPs formed stronger biofilms once the MPs were removed, associated with changes in motility. Thus, we find that MPs also select for cells that are better at forming biofilms, which can lead to recalcitrant infections in the environment and healthcare setting. Our study highlights the immediate need for comprehensive environmental management strategies to mitigate the risk posed by MPs. ImportanceAntimicrobial resistance is one of the worlds most pressing global health crises, with an estimated 10 million deaths per year forecasted by 2050. With the pipeline of antibiotics running dry, it is imperative that mitigation strategies understand the mechanisms that drive the genesis of antimicrobial resistance. One emerging dimension of antimicrobial resistance is the environment. This study highlights the relationship between a widespread environmental pollutant, (MPs), and the rise of drug-resistant bacteria. While it is known that MPs facilitate resistance through several modes (biofilm formation, plastic adsorption rates, etc.), this study fills the knowledge gap on how different types of MPs are contributing to antimicrobial resistance.

microbiology↗

Evolving a High-Performance Terminal Deoxynucleotidyl Transferase for Enzymatic DNA Synthesis

Enzymatic DNA synthesis, using stepwise nucleotide addition catalyzed by template-independent polymerases, promises higher efficiency, quality, and sustainability than todays industry standard phosphoramidite-based processes. We report on the directed evolution of a terminal deoxynucleotidyl transferase that uses 3-phosphate blocked dNTPs to control the polymerization reaction and demonstrates high activity for these modified substrates and improved template promiscuity and thermostability.

bioengineering↗

Endothelial cells secrete small extracellular vesicles bidirectionally containing distinct cargo to uniquely reprogram vascular cells in the circulation and vessel wall

Rationale: Extracellular vesicles (EVs) contain bioactive cargo including microRNAs (miRNAs) and proteins that are released by cells as a form of cell-cell communication. Endothelial cells (ECs) form the innermost lining of all blood vessels and thereby interface with cells in the circulation as well as cells residing in the vascular wall. It is unknown whether ECs have the capacity to release EVs capable of governing recipient cells within two separate compartments, and how this is affected by endothelial activation commonly seen in atheroprone regions. Objective: Given their boundary location, we propose that ECs utilize bidirectional release of distinct EV cargo in quiescent and activated states to communicate with cells within the circulation and blood vessel wall. Methods and Results: EVs were isolated from primary human aortic endothelial cells (ECs) (+/- IL-1{beta} activation), quantified, and analysed by miRNA transcriptomics and proteomics. Compared to quiescent ECs, activated ECs increased EV release, with miRNA and protein cargo that were related to atherosclerosis. RNA sequencing of EV-treated monocytes and smooth muscle cells (SMCs) revealed that EVs from activated ECs altered pathways that were pro-inflammatory and atherogenic. Apical and basolateral EV release was assessed using ECs on transwells. ECs released more EVs apically, which increased with activation. Apical and basolateral EV cargo contained distinct transcriptomes and proteomes that were altered by EC activation. Notably, basolateral EC-EVs displayed greater changes in the EV secretome, with pathways specific to atherosclerosis. In silico analysis determined that compartment-specific cargo released by the apical and basolateral surfaces of ECs can reprogram monocytes and SMCs, respectively. Conclusions: The demonstration that ECs are capable of polarized EV cargo loading and directional EV secretion reveals a novel paradigm for endothelial communication, which may ultimately enhance our ability to design endothelial-based therapeutics for cardiovascular diseases such as atherosclerosis where ECs are persistently activated. Non-standard Abbreviations and Acronyms O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=128 SRC="FIGDIR/small/538787v1_ufig1.gif" ALT="Figure 1"> View larger version (41K): org.highwire.dtl.DTLVardef@8e62dforg.highwire.dtl.DTLVardef@1fd4adeorg.highwire.dtl.DTLVardef@3e4433org.highwire.dtl.DTLVardef@1efa1a2_HPS_FORMAT_FIGEXP M_FIG C_FIG Graphical abstract: Polarized endothelial extracellular vesicle communication with luminal and abluminal vascular cellsEndothelial cell small extracellular vesicle (EC-EV) release from apical (luminal) and basolateral (abluminal) surfaces in quiescence and after endothelial activation. Quiescent EC-EVs are depicted in blue (bright blue=apical, light blue=basolateral), while activated EC-EVs are depicted in red (bright red=apical, light red=basolateral). Luminal monocyte is represented in purple with upregulation of pro-inflammatory transcripts (bright purple) after uptake of activated EC-EVs from the apical surface, compared to uptake of quiescent apical EC-EVs (light purple). Basolateral EC-EVs are taken up by an abluminal resident smooth muscle cell depicted in yellow. Smooth muscle cell uptake of activated basolateral EC-EVs with upregulation of pro-inflammatory/pro-atherogenic transcripts (bright yellow), as compared to uptake of quiescent EC-EVs (light yellow).

cell biology↗

Impact of Zinc Pre-exposure on de novo Antibiotic Resistance Development

Antimicrobial resistance (AMR) is a global health crisis that is currently predicted to worsen. While the impact of improper antibiotics is an established driver, much less is known on the impacts of metal supplements. Here, we specifically probe the impact of zinc (Zn) on AMR. In conflict settings where diarrhea disease cases are high, Zn is both given as a supplement for treatment of these diseases prior to use of antibiotics such as ciprofloxacin and is associated with weapons of war. In this study, we find that the order with which E. coli is exposed to zinc impacts resistance development, with increasing pre-exposure time leading to accelerated ciprofloxacin resistance, while combined exposure of zinc with ciprofloxacin delays ciprofloxacin resistance. We did not find evidence that zinc pre-exposure leads to genetic changes or change in antibiotic tolerance, though it does increase both the lag phase and doubling time of E. coli, suggesting the mechanism may be due to changes in gene expression. While the zinc phenotype behavior is not permeant and would no longer be observed if ciprofloxacin exposure did not occur right after zinc pre-exposure, the elevated MIC phenotype resulting from the zinc pre-exposure was more stable than the zinc phenotype. These results are important as they highlight the need to reexamine the clinical role of zinc in treating diarrheal diseases and assess if changes in resistance development observed in vitro are also observed in vivo. ImportanceAntimicrobial resistance (AMR) is a global problem. According to a 2014 Review on Antimicrobial Resistance, it is projected to result in several million deaths by 2050 (Review on Antimicrobial Resistance, Tackling a Crisis for the Health and Wealth of Nations, 2014). While the improper usage of antibiotic treatments is an accepted driver of AMR, little work has focused on how non-antibiotic medication, such as supplements, might impact this when combined with antibiotics. One supplement of interest is the heavy metal zinc which is used in conjunction with ciprofloxacin to treat diarrheal diseases in children. We find that the order and duration of zinc exposure has significant impact on resistance development. More specifically, although the combined presence of zinc and ciprofloxacin delays the onset of resistance, when used successively as they often are in practice, zinc pre-exposure followed by ciprofloxacin exposure results in faster resistance development.

microbiology↗

Effects of Antibiotic Interaction on Antimicrobial Resistance Development in Wastewater

While wastewater is understood to be a critically important reservoir of antimicrobial resistance due to the presence of multiple antibiotic residues from industrial and agricultural runoff, there is little known about the effects of antibiotic interactions in the wastewater on the development of resistance. We worked to fill this gap in quantitative understanding of antibiotic interaction in constant flow environments by experimentally monitoring E. coli populations under subinhibitory concentrations of combinations of antibiotics with synergistic, antagonistic, and additive interactions. We then used these results to expand our previously developed computational model to account for the complex effects of antibiotic interaction. We found that while E. coli populations grown in additively interacting antibiotic combinations grew predictably according to the previously developed model, those populations grown under synergistic and antagonistic antibiotic conditions exhibited significant differences from predicted behavior. E. coli populations grown in the condition with synergistically interacting antibiotics developed less resistance than predicted, indicating that synergistic antibiotics may have a suppressive effect on antimicrobial resistance development. Furthermore E. coli populations grown in the condition with antagonistically interacting antibiotics showed an antibiotic ratio-dependent development of resistance, suggesting that not only antibiotic interaction, but relative concentration is important in predicting resistance development. These results provide critical insight for quantitatively understanding the effects of antibiotic interactions in wastewater and provide a basis for future studies in modelling resistance in these environments. ImportanceAntimicrobial resistance (AMR) is a growing global threat to public health expected to impact 10 million people by 2050, driving mortality rates globally and with a disproportionate effect on low- and middle-income countries. Communities in proximity to wastewater settings and environmentally contaminated surroundings are at particular risk due to resistance stemming from antibiotic residues from industrial and agricultural runoff. Currently, there is a limited quantitative and mechanistic understanding of the evolution of AMR in response to multiple interacting antibiotic residues in constant flow environments. Using an integrated computational and experimental methods, we find that interactions between antibiotic residues significantly affect the development of resistant bacterial populations.

bioengineering↗

Molecular and connectomic vulnerability shape cross-disorder cortical abnormalities

Numerous brain disorders demonstrate structural brain abnormalities, which are thought to arise from molecular perturbations or connectome miswiring. The unique and shared contributions of these molecular and connectomic vulnerabilities to brain disorders remain unknown, and has yet to be studied in a single multi-disorder framework. Using MRI morphometry from the ENIGMA consortium, we construct maps of cortical abnormalities for thirteen neurodevelopmental, neurological, and psychiatric disorders from N = 21 000 patients and N = 26 000 controls, collected using a harmonized processing protocol. We systematically compare cortical maps to multiple micro-architectural measures, including gene expression, neurotransmitter density, metabolism, and myelination (molecular vulnerability), as well as global connectomic measures including number of connections, centrality, and connection diversity (connectomic vulnerability). We find that regional molecular vulnerability and macroscale brain network architecture interact to drive the spatial patterning of cortical abnormalities in multiple disorders. Local attributes, particularly neurotransmitter receptor profiles, constitute the best predictors of both disorder-specific cortical morphology and cross-disorder similarity. Finally, we find that cross-disorder abnormalities are consistently subtended by a small subset of network epicentres in bilateral sensory-motor, medial temporal lobe, precuneus, and superior parietal cortex. Collectively, our results highlight how local biological attributes and global connectivity jointly shape cross-disorder cortical abnormalities.

neuroscience↗

Condensate-mediated reactivation of mumps virus infection under stress

Many viruses can establish long-term persistent infections in the human host and cause chronic diseases. Here we combine cell biology, whole-cell proteomics and cryo-electron tomography to uncover how cellular stress disrupts the host-virus equilibrium in persistent infection and induces viral replication, using a model of negative-stranded RNA viruses, the mumps virus. We show that phosphorylation of the largely disordered viral phosphoprotein coincides with increased partitioning of viral polymerase into pre-formed liquid-like condensates and the formation of a stable replication machinery. By obtaining the first atomic models for the authentic mumps virus nucleocapsid, we elucidate a concomitant conformational change that exposes the viral genome to its replication machinery. These events that occur within viral condensates upon stress, together with concerted down-regulation of the host antiviral defense, provide an environment that supports up-regulation of viral replication and constitute a stress-mediated switch that disrupts the host-virus equilibrium in persistent infection. In BriefA multi-scale approach uncovers molecular and structural basis of how cellular stress provokes activation of persistent viral infection mediated by biomolecular condensates.

cell biology↗

Computational Model to Quantify the Growth of Antibiotic Resistant Bacteria in Wastewater

Although wastewater and sewage systems are known to be significant reservoirs of antibiotic resistant bacterial populations and periodic outbreaks of drug resistant infection, there is little quantitative understanding of the drivers behind resistant population growth in these settings. In order to fill this gap in quantitative understanding of the development of antibiotic resistant infections in wastewater, we have developed a mathematical model synthesizing many known drivers of antibiotic resistance in these settings to help predict the growth of resistant populations in different environmental scenarios. A number of these drivers of drug resistant infection outbreak including antibiotic residue concentration, antibiotic interaction, chromosomal mutation and horizontal gene transfer, have not previously been integrated into a single computational model. We validated the outputs of the model with quantitative studies conducted on the eVOLVER continuous culture platform. Our integrated model shows that low levels of antibiotic residues present in wastewater can lead to increased development of resistant populations, and the dominant mechanism of resistance acquisition in these populations is horizontal gene transfer rather than acquisition of chromosomal mutations. Additionally, we found that synergistic antibiotic interactions lead to increased resistant population growth. These findings, consistent with recent experimental and field studies, provide new quantitative knowledge on the evolution of antibiotic resistant bacterial reservoirs, and the model developed herein can be adapted for use as a prediction tool in public health policy making, particularly in low income settings where water sanitation issues remain widespread and disease outbreaks continue to undermine public health efforts. ImportanceThe rate at which antimicrobial resistance (AMR) has developed and spread throughout the world has increased in recent years, and according to the Review on Antimicrobial Resistance in 2014 it is suggested that the current rate will lead several million people AMR-related deaths by 205025. One major reservoir of resistant bacterial populations that has been linked to outbreaks of drug resistant bacterial infections, but is not well understood, is in wastewater settings, where antibiotic pollution is often present. Using ordinary differential equations incorporating several known drivers of resistance in wastewater, we find that interactions between antibiotic residues and horizontal gene transfer significantly affect the growth of resistant bacterial reservoirs.

bioengineering↗

Sex-Dependent Age Trajectories of Subcortical Brain Structures: Analysis of Large-Scale Percentile Models and Shape Morphometry

Modeling of structural brain variation over the lifespan is important to better understand factors contributing to healthy aging and risk for neurological conditions such as Alzheimers disease. Even so, we lack normative data on brain morphometry across the adult lifespan in large, well-powered samples. Here, in a large population-based sample of 26,440 adults from the UK Biobank (age: 44-81 yrs.), we created normative percentile charts for MRI-derived subcortical volumes. Next, we investigated associations between these morphometric measures and the strongest known genetic risk factor for late-onset Alzheimers disease (APOE genotype) and mapped the spatial distribution of age-by-sex interactions using computational surface mesh modeling and shape analysis. Vertex-wise shape mapping supplements traditional gross volumetric approaches to reveal finer-grained variations across functionally important brain subcompartments. Normative curves revealed volumetric loss with age, as expected, for all subcortical brain structures except for the lateral ventricles, which expanded with age. Surprisingly, no volumetric associations with APOE genotype were detected, despite the very large sample size. Age-related trajectories for volumes differed in women versus men, and surface-based statistical maps revealed the spatial distribution of the age-by-sex interaction. Subcortical volumes declined faster in men than women over the full age range, but after age 60, fewer structures showed sex-dependent trajectories, indicating similar volumetric changes in older men and women. Large-scale statistical modeling of age effects on brain structures may drive new insights into individual differences in brain aging and help to identify factors that promote healthy brain aging and risk for disease.

neuroscience↗

Greater male than female variability in regional brain structure across the lifespan

For many traits, males show greater variability than females, with possible implications for understanding sex differences in health and disease. Here, the ENIGMA (Enhancing Neuro Imaging Genetics through Meta-Analysis) Consortium presents the largest-ever mega-analysis of sex differences in variability of brain structure, based on international data spanning nine decades of life. Subcortical volumes, cortical surface area and cortical thickness were assessed in MRI data of 16,683 healthy individuals 1-90 years old (47% females). We observed significant patterns of greater male than female between-subject variance for all subcortical volumetric measures, all cortical surface area measures, and 60% of cortical thickness measures. This pattern was stable across the lifespan for 50% of the subcortical structures, 70% of the regional area measures, and nearly all regions for thickness. Our findings that these sex differences are present in childhood implicate early life genetic or gene-environment interaction mechanisms. The findings highlight the importance of individual differences within the sexes, that may underpin sex-specific vulnerability to disorders.

neuroscience↗