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Lou, M.

Publications and source records attributed to Lou, M..

11 recordsLinked to original sources

Systematic benchmarking of multi-modal approaches for tumor-naive ctDNA detection and quantification

Longitudinal monitoring of circulating tumor DNA (ctDNA) has emerged as a promising framework for characterizing treatment response dynamics in cancer. Scalable tumor-naive approaches for quantifying ctDNA often involve whole-genome sequencing (WGS) or DNA methylation profiling, but their comparative performance and capacity for complementary integration remain poorly understood. Here we systematically benchmarked tumor-naive WGS- and methylation-based ctDNA quantification methods using plasma from 150 patients with colorectal, lung and breast cancer. Using paired high-depth WGS and EM-seq data, we generated 40,000 in silico samples and evaluated detection accuracy, limits of detection (LoD) and quantification (LoQ) across cancer types and sequencing depths (0.1x-30x). We further assessed single- and multimodal method combinations, identifying conditions under which integrated approaches enhance analytical performance for detection and quantification relative to single modalities. This benchmark delineates key performance trade-offs and provides a practical framework to support method development and guide future research applications in ctDNA-based biomarker studies.

bioinformatics↗

Connections across regional glymphatic clearance, neural activity and amyloid-β deposition in cortex

Neural activity inevitably produces waste, which promotes neurodegeneration with topographic features. The glymphatic system is important for waste clearance. However, the spatial characteristics of glymphatic clearance across cortex and whether it interplays with neural activity in contribution to amyloidosis in human remain unexplored. Here, by intrathecal administration of gadolinium-based contrast agents, glymphatic influx and clearance patterns across cortex in 96 participants are depicted via Glymphatic MRI. Analyses integrating post-mortem transcriptomic profiles from Allen Human Brain Atlas indicate that, genes related with excitatory and inhibitory neurons, and pathways engaging in synaptic function were enriched in regions with faster glymphatic clearance. FALFF was calculated from resting-state fMRI to represent neural activity. At the regional level, based on a subgroup with rs-fMRI (N = 15), regional glymphatic clearance was positively coupled with spontaneous neural activity. Mismatch index, reflecting decoupling between spontaneous neural activity and glymphatic clearance function, turned out to be positively associated with regional severity of amyloidosis using open-source 11C-PiB dataset. Together, this study for the first time demonstrates the intricate interplays between neural activity and glymphatic dynamics from transcriptional to physiological level. The mismatch between these two processes may serve as an undescribed comprehensive mechanism promoting regional vulnerability to proteopathy and subsequent neurodegeneration in cortex.

neuroscience↗

Skull Bone Marrow Drainage and Its Associations with Inflammation, Sleep Quality, and Cognitive Performance

BackgroundRecent studies using human craniotomy samples and murine models have revealed channels that connect the inner skull cortex to the skull marrow cavities. While cerebrospinal fluid (CSF) tracer access to skull bone marrow has been described in CSF circulation disorders, evidence on regional patterns and clinical correlates in broader clinical cohorts is limited. MethodsThree-dimensional imaging was performed at baseline, 4.5, 15, and 39 hours post-gadolinium administration in 87 patients with neurological conditions. Signal changes in skull bone marrow near the superior sagittal sinus, lateral fissure, and cisterna magna were recorded. CSF drainage function was characterized as the percentage changes in the signal unit ratio within the skull bone marrow from baseline to time points post administration of gadolinium. ResultsThe tracer drained from CSF into the skull bone marrow, highlighting the drainage variations nearby different regions. Reduced drainage was associated with female sex, hypertension, diabetes, and elevated neutrophil levels (p < 0.05). Drainage near the superior sagittal sinus was inversely associated with sleep quality and positively associated with cognitive scores, and partially accounted for the association of sleep quality with cognitive function (indirect effect {Delta}{beta} = -0.092; bootstrap 95% CI -0.195 to -0.004; proportion mediated {approx} 38%). ConclusionThese results support the presence of skull bone marrow adjacent routes for CSF tracer movement and suggest that skull bone marrow tracer dynamics relate to systemic inflammation, sleep quality, and cognitive performance in this clinical cohort.

neuroscience↗

Relationships between phenotypic differences in punishment behaviour and prefrontal cortex network engagement

Avoiding actions with negative consequences is fundamental to adaptive behaviour, yet individuals differ drastically in their tendencies to avoid to punishment. Using a conditioned punishment task in male and female rats, we replicate findings of a bimodal distribution of punishment avoidance, and identify four distinct behavioural phenotypes (Sensitive, Hypersensitive, Insensitive, Generalised) that differed in their punishment avoidance, unpunished reward-seeking, and Pavlovian fear. We examined how these phenotypic differences related to c-Fos (transcriptional activity marker) across prefrontal cortex (PFC) regions. While region-level c-Fos differences were minimal, covariance and graph-theoretic analyses revealed three functional PFC networks predominantly composed of medial PFC, ventrolateral PFC, or sensorimotor regions. Activity in the ventrolateral PFC network predicted punishment avoidance, while activity in the medial PFC network predicted generalised suppression during initial punishment learning. These findings suggest phenotypic differences in punishment sensitivity is underpinned by differential recruitment of distinct cortical networks that drive adaptive versus maladaptive responses to negative outcomes.

neuroscience↗

Dietary manipulation of intestinal microbes prolongs survival in a mouse model of Hirschsprung disease

Enterocolitis is a common and potentially deadly manifestation of Hirschsprung disease (HSCR) but disease mechanisms remain poorly defined. Unexpectedly, we discovered that diet can dramatically affect the lifespan of a HSCR mouse model (Piebald lethal, sl/sl) where affected animals die from HAEC complications. In the sl/sl model, diet alters gut microbes and metabolites, leading to changes in colon epithelial gene expression and epithelial oxygen levels known to influence colitis severity. Our findings demonstrate unrecognized similarity between HAEC and other types of colitis and suggest dietary manipulation could be a valuable therapeutic strategy for people with HSCR. AbstractHirschsprung disease (HSCR) is a birth defect where enteric nervous system (ENS) is absent from distal bowel. Bowel lacking ENS fails to relax, causing partial obstruction. Affected children often have "Hirschsprung disease associated enterocolitis" (HAEC), which predisposes to sepsis. We discovered survival of Piebald lethal (sl/sl) mice, a well-established HSCR model with HAEC, is markedly altered by two distinct standard chow diets. A "Protective" diet increased fecal butyrate/isobutyrate and enhanced production of gut epithelial antimicrobial peptides in proximal colon. In contrast, "Detrimental" diet-fed sl/sl had abnormal appearing distal colon epithelium mitochondria, reduced epithelial mRNA involved in oxidative phosphorylation, and elevated epithelial oxygen that fostered growth of inflammation-associated Enterobacteriaceae. Accordingly, selective depletion of Enterobacteriaceae with sodium tungstate prolonged sl/sl survival. Our results provide the first strong evidence that diet modifies survival in a HSCR mouse model, without altering length of distal colon lacking ENS. HighlightsO_LITwo different standard mouse diets alter survival in the Piebald lethal (sl/sl) mouse model of Hirschsprung disease, without impacting extent of distal colon aganglionosis (the region lacking ENS). C_LIO_LIPiebald lethal mice fed the "Detrimental" diet had many changes in colon epithelial transcriptome including decreased mRNA for antimicrobial peptides and genes involved in oxidative phosphorylation. Detrimental diet fed sl/sl also had aberrant-appearing mitochondria in distal colon epithelium, with elevated epithelial oxygen that drives lethal Enterobacteriaceae overgrowth via aerobic respiration. C_LIO_LIElimination of Enterobacteriaceae with antibiotics or sodium tungstate improves survival of Piebald lethal fed the "Detrimental diet". C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=94 SRC="FIGDIR/small/637436v1_ufig1.gif" ALT="Figure 1"> View larger version (15K): org.highwire.dtl.DTLVardef@d95251org.highwire.dtl.DTLVardef@1ab58caorg.highwire.dtl.DTLVardef@5260b0org.highwire.dtl.DTLVardef@49ce42_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Morphological brain alterations and morphological brain network disorganizations in heroin and methamphetamine abstinent patients

Heroin and methamphetamine are the two common types of drugs abused, which poses significant health risks. However, the neural mechanisms underlying the effects of drug addiction on human brain are unclear. In this study, we collected T1-weighted magnetic resonance imaging data from 26 heroin abstinent (HA) patients, 24 methamphetamine abstinent (MA) patients and 32 healthy controls. Four surface-based morphological features including cortical thickness (CT), fractal dimension (FD), gyrification index (GI), and sulcal depth (SD) were calculated, and further used to construct the morphological brain networks. We observed the common CT reductions of the right TE 1.0 and TE 1.2 and SD reductions of the right intermediate lateral area 20 for HA and MA patients, HA-specific CT reductions in the left area 2, and the MA-specific GI reductions in the left medial area 6 and right dorsomedial parietooccipital sulcus. For the morphological brain networks, HA patients exhibited the global disorganizations (higher shortest path length) in CT-based networks, whereas MA patients showed the disrupted nodal efficiency of the left medial area 38 in CT-based networks, the right caudal area 7 in GI-based networks, and the right inferior occipital gyrus in SD-based networks. Furthermore, the altered SD of HA patients and disrupted nodal efficiency of MA patients were associated with drug abuse-related clinical variables. Our findings suggest the morphological index-dependent effects of drug addiction on human brain morphology, and indicate the differential neural mechanism underlying heroin and methamphetamine abuses which attack the global and local information transfer of morphological brain networks, respectively.

neuroscience↗

Identity and Nature of Neural Stem Cells in the Adult Human Subventricular Zone

The existence of neural stem cells (NSCs) in adult human brain neurogenic regions remains unresolved. To address this, we created a cell atlas of the adult human subventricular zone (SVZ) derived from fresh neurosurgical samples using single-cell transcriptomics. We discovered 2 adult radial glia (RG)-like populations, aRG1 and aRG2. aRG1 shared features with fetal early RG (eRG) and aRG2 were transcriptomically similar to fetal outer RG (oRG). We also captured early neuronal and oligodendrocytic NSC states. We found that the biological programs driven by their transcriptomes support their roles as early-lineage NSCs. Finally, we show that these NSCs have the potential to transition between states and along lineage trajectories. These data reveal that multipotent NSCs reside in the adult human SVZ.

neuroscience↗

The lipid Gb3 promotes germinal center B cell responses and anti-viral immunity

Influenza viruses escape immunity due to rapid antigenic evolution, which requires vaccination strategies that allow for broadly protective antibody responses. Here, we demonstrate that the lipid globotriaosylceramide (Gb3) expressed on germinal center (GC) B cells is essential for the production of high-affinity antibodies. Mechanistically, Gb3 binds and disengages CD19 from its chaperone CD81 for subsequent translocation to the B cell receptor (BCR) complex to trigger signaling. Abundance of Gb3 amplifies the PI3-kinase/Akt/Foxo1 pathway to drive affinity maturation. Moreover, this lipid regulates MHC-II expression to increase diversity of T follicular helper (Tfh) and GC B cells reactive with subdominant epitopes. In influenza infection, Gb3 promotes broadly reactive antibody responses and cross-protection. Thus, we show that Gb3 determines affinity as well as breadth in B cell immunity and propose this lipid as novel vaccine adjuvant against viral infection. One Sentence SummaryGb3 abundance on GC B cells selects antibodies with high affinity and broad epitope reactivities, which are cross-protective against heterologous influenza infection.

immunology↗

Hyperglycosylation of prosaposin in tumor DCs promotes immune escape in cancer

Tumors develop strategies to evade immunity by suppressing antigen presentation. Here, we show that prosaposin drives CD8 T cell-mediated tumor immunity and that its hyperglycosylation in tumor DCs leads to cancer immune escape. We found that lysosomal prosaposin and its single saposin cognates mediated disintegration of tumor cell-derived apoptotic bodies to facilitate presentation of membrane-associated antigen and T cell activation. In the tumor microenvironment, TGF-{beta} induced hyperglycosylation of prosaposin and its subsequent secretion, which ultimately caused depletion of lysosomal saposins. In melanoma patients, we found similar prosaposin hyperglycosylation in tumor-associated DCs, and reconstitution with prosaposin rescued activation of tumor-infiltrating T cells. Targeting tumor DCs with recombinant prosaposin triggered cancer protection and enhanced immune checkpoint therapy. Our studies demonstrate a critical function of prosaposin in tumor immunity and escape and introduce a novel principle of prosaposin-based cancer immunotherapy. One Sentence SummaryProsaposin facilitates antigen cross-presentation and tumor immunity and its hyperglycosylation leads to immune evasion.

immunology↗

Impaired peri-olfactory Cerebrospinal Fluid clearance mediated cognitive decline after dyssomnia

Animal experiments have demonstrated the dependency of CSF clearance function on age and sleep, which partially underlay the cognitive decline in the elderly. However, evidence is lacking in humans mainly due to limited method to assess CSF clearance function. We aimed to image CSF clearance pathways in human brain by dynamic MRI with intrathecal contrast agent as a CSF tracer. We performed T1-weighted and T2-fluid attenuated inversion recovery imaging with equal sequence parameters before and at multiple time points after intrathecal injection of contrast agent to visualize the putative meningeal lymphatic pathway, peri-olfactory nerve pathway and peri-optic nerve pathway. We defined the CSF clearance function as the percentage change in signal unit ratio of critical locations in these pathways from baseline to 39 hours after intrathecal injection. CSF clearance through the putative meningeal lymphatic and peri-neural pathways were clearly visualized in all 85 patients. The CSF clearance function of meningeal lymphatic and peri-neural pathways were reduced with aging (all P < 0.05). The CSF clearance function through peri-olfactory nerve pathway was positive correlated with sleep quality and cognitive function (both P < 0.05). Moreover, the CSF clearance function through peri-olfactory nerve pathway mediated the association of sleep quality with cognitive function (percent change in {beta} [bootstrap 95% confidence interval]: 35% [-0.220, -0.003]). The study shows promise for dynamic MRI with intrathecal injection of contrast agent as a method to assess CSF clearance function through putative peri-neural pathways, and interprets the impaired clearance through putative peri-olfactory nerve pathway may explain the cognitive decline in patients with dyssomnia.

neuroscience↗

Superficial white matter microstructure affects processing speed in cerebral small vessel disease

White matter hyperintensities (WMH) are a typical feature of cerebral small vessel disease (CSVD). This condition contributes to about 50% of dementias worldwide, a massive health burden in aging. Microstructural alterations in the deep white matter (DWM) have been widely examined in CSVD. However, little is known about abnormalities in the superficial white matter (SWM) and their relevance for processing speed, the main cognitive deficit in CSVD. In this paper, 141 patients with CSVD were studied. Processing speed was assessed by the completion time of the Trail Making Test Part A. White matter abnormalities were assessed by WMH burden (lesion volume on T2-FLAIR) and diffusion MRI, including DTI and free-water (FW) imaging microstructure measures. The results of our study indicate that the superficial white matter may play a particularly important role in cognitive decline in CSVD. SWM imaging measures resulted in a large contribution to processing speed, despite a relatively small WMH burden in the SWM. SWM FW had the strongest association with processing speed among all imaging markers and, unlike the other diffusion MRI measures, significantly increased between two patient subgroups with the lowest WMH burdens (possibly representing early stages of disease). When comparing two patient subgroups with the highest WMH burdens, the involvement of WMH in the SWM was accompanied by significant differences in processing speed and white matter microstructure. Given significant effects of WMH volume and regional FW on processing speed, we performed a mediation analysis. SWM FW was found to fully mediate the association between WMH volume and processing speed, while no mediation effect of DWM FW was observed. Overall, our findings identify SWM abnormalities in CSVD and suggest that the SWM has an important contribution to processing speed. Results indicate that FW in the SWM is a sensitive marker of microstructural changes associated with cognition in CSVD. This study extends the current understanding of CSVD-related dysfunction and suggests that the SWM, as an understudied region, can be a potential target for monitoring pathophysiological processes in future research.

neuroscience↗