Enhancing the Carbon Monoxide Oxidation Performance through Surface Defect Enrichment of Ceria-Based Supports for Platinum Catalyst.

Effective synthesis and application of single-atom catalysts on supports lacking enough defects remain a significant challenge in environmental catalysis. Herein, we present a universal defect-enrichment strategy to increase the surface defects of CeO2-based supports through H2 reduction pretreatment. The Pt catalysts supported by defective CeO2-based supports, including CeO2, CeZrOx, and CeO2/Al2O3 (CA), exhibit much higher Pt dispersion and CO oxidation activity upon reduction activation compared to their counterpart catalysts without defect enrichment. Specifically, Pt is present as embedded single atoms on the CA support with enriched surface defects (CA-HD) based on which the highly active catalyst showing embedded Pt clusters (PtC) with the bottom layer of Pt atoms substituting the Ce cations in the CeO2 surface lattice can be obtained through reduction activation. Embedded PtC can better facilitate CO adsorption and promote O2 activation at PtC-CeO2 interfaces, thereby contributing to the superior low-temperature CO oxidation activity of the Pt/CA-HD catalyst after activation.

Association of hemoglobin drift and outcomes in patients with aneurysmal subarachnoid hemorrhage.

The relationship between in-hospital hemoglobin (Hb) drift and outcomes in patients undergoing surgical clipping for aneurysmal subarachnoid hemorrhage (aSAH) is not well studied. This study aims to investigate the association between Hb drift and mortality in this patient population. We conducted a cohort study encompassing adult patients diagnosed with aSAH who were admitted to a university hospital. These patients were stratified into distinct groups based on their Hb drift levels. We employed logistic and Cox proportional hazard models to assess the relationship between Hb drift and outcomes. Additionally, propensity score matching (PSM) was utilized to ensure comparability between patient groups. The discriminative performance of different models was evaluated using C-statistics, integrated discrimination improvement (IDI), and net reclassification improvement (NRI). Overall, our cohort comprised 671 patients, of whom 165 (24.6%) demonstrated an in-hospital Hb drift exceeding 25%. The analyses revealed elevated Hb drift was independently associated with higher likelihood of follow-up mortality (aOR: 3.29, 95% CI: 1.65 to 6.56; P = 0.001) and in-hospital mortality (aOR: 3.44, 95% CI: 1.55 to 7.63; P = 0.002). PSM analysis yielded similar results. Additionally, patients with Hb drift exhibited a notable decrease in survival rate compared to those without Hb drift (aHR: 3.99, 95% CI 2.30 to 6.70; P < 0.001). Furthermore, the inclusion of Hb drift significantly improved the C-statistic (P = 0.037), IDI (2.78%; P = 0.004) and NRI metrics (41.86%; P < 0.001) for mortality prediction. In summary, our results highlight that an in-hospital Hb drift exceeding 25% serves as an independent predictor of mortality in patients who have undergone surgical clipping for aSAH.

Defect-Driven Configurational Entropy in the High-Entropy Oxide Li1.5MO3-δ.

Layered lithiated oxides are promising materials for next generation Li-ion battery cathode materials; however, instability during cycling results in poor performance over time compared to the high capacities theoretically possible with these materials. Here we report the characterizations of a Li1.47Mn0.57Al0.13Fe0.095Co0.105Ni0.095O2.49 high-entropy layered oxide (HELO) with the Li2MO3 structure where M = Mn, Al, Fe, Co, and Ni. Using electron microscopy and X-ray spectroscopy, we identify a homogeneous Li2MO3 structure stabilized by the entropic contribution of oxygen vacancies. This defect-driven entropy would not be attainable in the LiMO2 structure sometimes observed in similar materials as a secondary phase owing to the presence of fewer O sites and a 3+ oxidation state for the metal site; instead, a Li2-γMO3-δ is produced. Beyond Li2MO3, this defect-driven entropy approach to stabilizing novel compositions and phases can be applied to a wide array of future cathode materials including spinel and rock salt structures.

S-Block Metal Mg-Mediated Co─N─C as Efficient Oxygen Electrocatalyst for Durable and Temperature-Adapted Zn-Air Batteries.

In the quest to enhance Zn-air batteries (ZABs) for operating across a wide spectrum of temperatures, synthesizing robust oxygen electrocatalysts is paramount. Conventional strategies focusing on orbital hybridization of d-d and p-d aim to moderate the excessive interaction between the d-band of the transition metal active site and oxygen intermediate, yet often yield suboptimal performance. Herein, an innovative s-block metal modulation is reported to refine the electronic structure and catalytic behavior of Co─NC catalysts. Employing density functional theory (DFT) calculations, it is revealed that incorporating Mg markedly depresses the d-band center of Co sites, thereby fine-tuning the adsorption energy of the oxygen reduction reaction (ORR) intermediate. Consequently, the Mg-modified Co─NC catalyst (MgCo─NC) unveils remarkable intrinsic ORR activity with a significantly reduced activation energy (Ea) of 10.0 kJ mol-1, outstripping the performance of both Co─NC (17.6 kJ mol-1), benchmark Pt/C (15.9 kJ mol-1), and many recent reports. Moreover, ZABs outfitted with the finely tuned Mg0.1Co0.9─NC realize a formidable power density of 157.0 mW cm-2, paired with an extremely long cycle life of 1700 h, and an exceptionally minimal voltage gap decay rate of 0.006 mV h-1. Further, the Mg0.1Co0.9─NC-based flexible ZAB presents a mere 2% specific capacity degradation when the temperature fluctuates from 25 to -20 °C, underscoring its robustness and suitability for practical deployment in diverse environmental conditions.

Psychosocial factors affect the occurrence of nonsuicidal self-injury in adolescents with major depressive disorder through chain mediation.

In the adolescent group, about half of adolescents with major depressive disorder (MDD) have NSSI. Psychosocial factors are associated with the development of NSSI. Clarifying the relationship between psychosocial factors and NSSI in adolescents with MDD can help us achieve early prevent. Demographic data, Hamilton Depression Scale-24 (HAMA24), childhood trauma questionnaire, emotional intelligence scale and interpersonal reactivity index were collected from 187 adolescents with MDD. Use ANOVA, Chi-square test, Binary Logistic Regression, Pearson correlation analysis, Mediation effect analysis and the Structural Equation Model for data analysis. The results of ANOVA showed that there was significant difference between the two groups in HAMD24 total score, impulsiveness, emotional intelligence, and empathy (p < 0.05). In the regression analysis, women, depression degree, motor impulsiveness (MI), personal distress (PD) and appraisal of other's emotions empathy were the risk factors for MDD adolescents to produce NSSI behavior. Among the indicators that were significantly related to MDD and NSSI, MI and PD mediate the relationship between MDD and NSSI. The structural equation model showed that MDD, PD and MI had a direct impact on NSSI, but PD and MI had multiple intermediary effected in the relationship between MDD and NSSI. Emotional intelligence, emotional neglect and cognitive impulsiveness indirectly affected the occurrence of NSSI behavior. Impulsiveness, personal distress, emotional neglect, and emotional intelligence are important risk factors that affect NSSI behavior in adolescents with MDD, and they affect the occurrence of NSSI in adolescents with MDD through chain mediation.

Potential Biomarkers in Cerebrospinal Fluid and Plasma for Dementia.

Background: The identification of biomarkers for different dementias in plasma and cerebrospinal fluid (CSF) has made substantial progress. However, they are observational studies, and there remains a lack of research on dementias with low incidence rates. Objective: We performed a comprehensive Mendelian randomization to identify potential biomarkers for different dementia type. Methods: The summary-level datasets encompassed 734 plasma and 154 cerebrospinal fluid proteins sourced from recently published genome-wide association studies (GWAS). Summary statistics for different dementias, including any dementia (refering to any type of dementia symptoms, 218,792 samples), Alzheimer's disease (AD, 63,926 samples), vascular dementia (212,389 samples), frontotemporal dementia (3,024 samples), dementia with Lewy bodies (DLB, 6,618 samples), and dementia in Parkinson's disease (216,895 samples), were collected from large GWAS. The primary method is inverse variance weighting, with additional sensitivity analyses conducted to ensure the robustness of the findings. Results: The molecules released into CSF, namely APOE2 for any dementia, APOE2 and Siglec-3 for AD, APOE2 for vascular dementia, and APOE2 for DLB, might be potential biomarkers. CD33 for AD and SNCA for DLB in plasma could be promising biomarkers. Conclusions: This is the first study to integrate plasma and CSF proteins to identify potential biomarkers for different dementias.

Filling the gaps in icosahedral superatomic metal clusters.

Chemically modified superatoms have emerged as promising candidates in the new periodic table, in which Au13 and its doped M n Au13- n have been widely studied. However, their important counterpart, Ag13 artificial element, has not yet been synthesized. In this work, we report the synthesis of Ag13 nanoclusters using strong chelating ability and rigid ligands, that fills the gaps in the icosahedral superatomic metal clusters. After further doping Ag13 template with different degrees of Au atoms, we gained insight into the evolution of their optical properties. Theoretical calculations show that the kernel metal doping can modulate the transition of the excited-state electronic structure, and the electron transfer process changes from local excitation (LE) to charge transfer (CT) to LE. This study not only enriches the families of artificial superatoms, but also contributes to the understanding of the electronic states of superatomic clusters.

Efficient Initialization of Fluxonium Qubits based on Auxiliary Energy Levels.

Fast and high-fidelity qubit initialization is crucial for low-frequency qubits such as fluxonium, and in applications of many quantum algorithms and quantum error correction codes. In a circuit quantum electrodynamics system, the initialization is typically achieved by transferring the state between the qubit and a short-lived cavity through microwave driving, also known as the sideband cooling process in atomic system. Constrained by the selection rules from the parity symmetry of the wave functions, the sideband transitions are only enabled by multiphoton processes which require multitone or strong driving. Leveraging the flux tunability of fluxonium, we circumvent this limitation by breaking flux symmetry to enable an interaction between a noncomputational qubit transition and the cavity excitation. With single-tone sideband driving, we realize qubit initialization with a fidelity exceeding 99% within a duration of 300 ns, robust against the variation of control parameters. Furthermore, we show that our initialization scheme has a built-in benefit in simultaneously removing the second-excited state population of the qubit, and can be easily incorporated into a large-scale fluxonium processor.

Nano- and microplastics drive the dynamic equilibrium of amoeba-associated bacteria and antibiotic resistance genes.

As emerging pollutants, microplastics have become pervasive on a global scale, inflicting significant harm upon ecosystems. However, the impact of these microplastics on the symbiotic relationship between protists and bacteria remains poorly understood. In this study, we investigated the mechanisms through which nano- and microplastics of varying sizes and concentrations influence the amoeba-bacterial symbiotic system. The findings reveal that nano- and microplastics exert deleterious effects on the adaptability of the amoeba host, with the magnitude of these effects contingent upon particle size and concentration. Furthermore, nano- and microplastics disrupt the initial equilibrium in the symbiotic relationship between amoeba and bacteria, with nano-plastics demonstrating a reduced ability to colonize symbiotic bacteria within the amoeba host when compared to their microplastic counterparts. Moreover, nano- and microplastics enhance the relative abundance of antibiotic resistance genes and heavy metal resistance genes in the bacteria residing within the amoeba host, which undoubtedly increases the potential transmission risk of both human pathogens and resistance genes within the environment. In sum, the results presented herein provide a novel perspective and theoretical foundation for the study of interactions between microplastics and microbial symbiotic systems, along with the establishment of risk assessment systems for ecological environments and human health.

Copper stress shapes the dynamic behavior of amoebae and their associated bacteria.

Amoeba-bacteria interactions are prevalent in both natural ecosystems and engineered environments. Amoebae, as essential consumers, hold significant ecological importance within ecosystems. Besides, they can establish stable symbiotic associations with bacteria. Copper plays a critical role in amoeba predation by either killing or restricting the growth of ingested bacteria in phagosomes. However, certain symbiotic bacteria have evolved mechanisms to persist within the phagosomal vacuole, evading antimicrobial defenses. Despite these insights, the impact of copper on the symbiotic relationships between amoebae and bacteria remains poorly understood. In this study, we investigated the effects of copper stress on amoebae and their symbiotic relationships with bacteria. Our findings revealed that elevated copper concentration adversely affected amoeba growth and altered cellular fate. Symbiont type significantly influenced the responses of the symbiotic relationships to copper stress. Beneficial symbionts maintained stability under copper stress, but parasitic symbionts exhibited enhanced colonization of amoebae. Furthermore, copper stress favored the transition of symbiotic relationships between amoebae and beneficial symbionts toward the host's benefit. Conversely, the pathogenic effects of parasitic symbionts on hosts were exacerbated under copper stress. This study sheds light on the intricate response mechanisms of soil amoebae and amoeba-bacteria symbiotic systems to copper stress, providing new insights into symbiotic dynamics under abiotic factors. Additionally, the results underscore the potential risks of copper accumulation in the environment for pathogen transmission and biosafety.

YAP1 inhibits the senescence of alveolar epithelial cells by targeting Prdx3 to alleviate pulmonary fibrosis.

The senescence of alveolar type II (AT2) cells impedes self-repair of the lung epithelium and contributes to lung injury in the setting of idiopathic pulmonary fibrosis (IPF). Yes-associated protein 1 (YAP1) is essential for cell growth and organ development; however, the role of YAP1 in AT2 cells during pulmonary fibrosis is still unclear. YAP1 expression was found to be downregulated in the AT2 cells of PF patients. Deletion of YAP1 in AT2 cells resulted in lung injury, exacerbated extracellular matrix (ECM) deposition, and worsened lung function. In contrast, overexpression of YAP1 in AT2 cells promoted alveolar regeneration, mitigated pulmonary fibrosis, and improved lung function. In addition, overexpression of YAP1 alleviated bleomycin (BLM) -induced senescence of alveolar epithelial cells both in vivo and in vitro. Moreover, YAP1 promoted the expression of peroxiredoxin 3 (Prdx3) by directly interacting with TEAD1. Forced expression of Prdx3 inhibited senescence and improved mitochondrial dysfunction in BLM-treated MLE-12 cells, whereas depletion of Prdx3 partially abrogated the protective effect of YAP1. Furthermore, overexpression of Prdx3 facilitated self-repair of the injured lung and reduced ECM deposition, while silencing Prdx3 attenuated the antifibrotic effect of YAP1. In conclusion, this study demonstrated that YAP1 alleviates lung injury and pulmonary fibrosis by regulating Prdx3 expression to improve mitochondrial dysfunction and block senescence in AT2 cells, revealing a potential novel therapeutic strategy for pulmonary fibrosis.

Single-Cell Transcriptomics Revealed White Matter Repair Following Subarachnoid Hemorrhage.

Existing research indicates the potential for white matter injury repair during the subacute phase following subarachnoid hemorrhage (SAH). However, elucidating the role of brain cell subpopulations in the acute and subacute phases of SAH pathogenesis remains challenging due to the cellular heterogeneity of the central nervous system. In this study, single-cell RNA sequencing was conducted on SAH model mice to delineate distinct cell populations. Gene Set Enrichment Analysis was performed to identify involved pathways, and cellular interactions were explored using the CellChat package in R software. Validation of the findings involved a comprehensive approach, including magnetic resonance imaging, immunofluorescence double staining, and Western blot analyses. This study identified ten major brain clusters with cell type-specific gene expression patterns. Notably, we observed infiltration and clonal expansion of reparative microglia in white matter-enriched regions during the subacute stage after SAH. Additionally, microglia-associated pleiotrophin (PTN) was identified as having a role in mediating the regulation of oligodendrocyte precursor cells (OPCs) in SAH model mice, implicating the activation of the mTOR signaling pathway. These findings emphasize the vital role of microglia-OPC interactions might occur via the PTN pathway, potentially contributing to white matter repair during the subacute phase after SAH. Our analysis revealed precise transcriptional changes in the acute and subacute phases after SAH, offering insights into the mechanism of SAH and for the development of drugs that target-specific cell subtypes.

Resveratrol Alleviates Arsenic Exposure-Induced Liver Fibrosis in Rats by Inhibiting Hepatocyte Senescence.

Arsenic is an environmental pollutant that has garnered considerable attention from the World Health Organization. Liver fibrosis is an advanced pathological stage of liver injury that can be caused by chronic arsenic exposure and has the potential to be reversed to prevent cirrhosis and hepatic malignancies. However, effective treatment options are currently limited. Given the profibrogenic effect of hepatocyte senescence, we established a rat model of sub-chronic sodium arsenite exposure and investigated the ability of resveratrol (RSV), a potential anti-senescence agent, to ameliorate arsenic-induced liver fibrosis and elucidate the underlying mechanism from the perspective of hepatocyte senescence. The results demonstrated that RSV was capable of mitigating fibrosis phenotypes in rat livers, including the activation of hepatic stellate cell (HSC), the generation of extracellular matrix, and the deposition of collagen fibers in the liver vascular zone, which are all induced by arsenic exposure. Furthermore, as an activator of the longevity factor SIRT1, RSV antagonized the arsenic-induced inhibition of SIRT1 expression, thereby restoring the suppression of the senescence protein p16 by SIRT1. This prevented arsenic-induced hepatocyte senescence, manifesting as a decrease in telomere shortening and a reduction in the release of senescence-associated secretory phenotype (SASP)-related proteins. In conclusion, this study demonstrated that RSV counteracts arsenic-induced hepatocyte senescence and the release of SASP-related proteins by restoring the inhibitory effect of SIRT1 on p16, thereby suppressing the activation of fibrotic phenotypes and mitigating liver fibrosis. These findings provide new insights for understanding the mechanism of arsenic-induced liver fibrosis, and more importantly, they reveal novel potential interventional approaches.

Revealing the Nature of Binary-Phase on Structural Stability of Sodium Layered Oxide Cathodes.

The emergence of layered sodium transition metal oxides featuring a multiphase structure presents a promising approach for cathode materials in sodium-ion batteries, showcasing notably improved energy storage capacity. However, the advancement of cathodes with multiphase structures faces obstacles due to the limited understanding of the integrated structural effects. Herein, the integrated structural effects by an in-depth structure-chemistry analysis in the developed layered cathode system NaxCu0.1Co0.1Ni0.25Mn0.4Ti0.15O2 with purposely designed P2/O3 phase integration, are comprehended. The results affirm that integrated phase ratio plays a pivotal role in electrochemical/structural stability, particularly at high voltage and with the incorporation of anionic redox. In contrast to previous reports advocating solely for the enhanced electrochemical performance in biphasic structures, it is demonstrated that an inappropriate composite structure is more destructive than a single-phase design. The in situ X-ray diffraction results, coupled with density functional theory computations further confirm that the biphasic structure with P2:O3 = 4:6 shows suppressed irreversible phase transition at high desodiated states and thus exhibits optimized electrochemical performance. These fundamental discoveries provide clues to the design of high-performance layered oxide cathodes for next-generation SIBs.

Unrecoverable lattice rotation governs structural degradation of single-crystalline cathodes.

Transitioning from polycrystalline to single-crystalline nickel-rich cathodes has garnered considerable attention in both academia and industry, driven by advantages of high tap density and enhanced mechanical properties. However, cathodes with high nickel content (>70%) suffer from substantial capacity degradation, which poses a challenge to their commercial viability. Leveraging multiscale spatial resolution diffraction and imaging techniques, we observe that lattice rotations occur universally in single-crystalline cathodes and play a pivotal role in the structure degradation. These lattice rotations prove unrecoverable and govern the accumulation of adverse lattice distortions over repeated cycles, contributing to structural and mechanical degradation and fast capacity fade. These findings bridge the previous knowledge gap that exists in the mechanistic link between fast performance failure and atomic-scale structure degradation.

Hydrothermal synthesis of high crystallinity ZSM-5 zeolite from coal gasification coarse slag and mother liquor circulation for efficient coal chemical wastewater purification.

A hydrothermal synthesis method was developed to produce high crystallinity ZSM-5 zeolite using coal gasification coarse slag (CGCS) as the raw material. Instead of the expensive NaOH(s.), Na2SiO3(s.) was utilized to activate, depolymerize, and recombine Si and Al elements in the CGCS. The mother liquor circulation technology was employed to recover and reuse raw materials and residual reagents (Na2SiO3(aq.) and TPABr), reducing waste emissions and enhancing resource utilization efficiency. The synthesized ZSM-5 had a specific surface area of 455.675 m2 g-1, pore volume of 0.284 cm3 g-1, and pore diameter of 2.496 nm. The influence of various factors on the morphology and crystallinity of ZSM-5 was investigated, resulting in the production of ZSM-5 with higher specific surface area and pore volume. Adsorption experiments showed that WU-ZSM-5 exhibited a removal efficiency of 85% for ammonia nitrogen (NH4+-N(aq.)), validating its effectiveness in coal chemical wastewater purification. The mother liquor recycling technology enabled zero-emission utilization of solid waste resources and improved the utilization rate of alkali and template to 90%. These results demonstrate the potential application of the developed method in the efficient treatment of coal chemical wastewater.

Triply Interlocked [2]catenanes: Rational Synthesis, Reversible Conversion Studies and Unprecedented Application in Photothermal Responsive Elastomer.

Triply interlocked [2]catenane complexes featuring two identical, mechanically interlocked units are extraordinarily rare chemical compounds, whose properties and applications remain open to detailed studies. Herein, we introduce the rational design of a new ligand precursor, L1, suitable for the synthesis of six triply interlocked [2]catenanes by coordination-driven self-assembly. The interlocked compounds can be reversibly converted into the corresponding simple triangular prism metallacage by addition of H2O or DMF solvents to their CH3OH solutions, thereby demonstrating the importance of π⋅⋅⋅π stacking and hydrogen bonding interactions in the formation of triply interlocked [2]catenanes. Moreover, extensive studies have been conducted to assess the remarkable photothermal conversion performance. Complex 6 a, exhibiting outstanding photothermal conversion performance (conversion efficiency in solution : 31.82 %), is used to prepare novel photoresponsive elastomer in combination with thermally activated liquid crystal elastomer. The resultant material displays robust response to near-infrared (NIR) laser and the capability of completely reforming the shape and reversible actuation, paving the way for the application of half-sandwich organometallic units in photo-responsive smart materials.

Causal association between circulating inflammatory cytokines and intracranial aneurysm and subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The causal association between inflammatory cytokines and the development of intracranial aneurysm (IA), unruptured IA (uIA) and subarachnoid hemorrhage (SAH) lacks clarity. METHODS: The summary-level datasets for inflammatory cytokines were extracted from a genome-wide association study of the Finnish Cardiovascular Risk in Young Adults Study and the FINRISK survey. The summary statistics datasets related to IA, uIA and SAH were obtained from the genome-wide association study meta-analysis of the International Stroke Genetics Consortium and FinnGen Consortium. The primary method employed for analysis was inverse variance weighting (false discovery rate), supplemented by sensitivity analyses to address pleiotropy and enhance robustness. RESULTS: In the International Stroke Genetics Consortium, 10, six and eight inflammatory cytokines exhibited a causal association with IA, uIA and SAH, respectively (false discovery rate, p < 0.05). In FinnGen datasets, macrophage Inflammatory Protein-1 Alpha (MIP_1A), MIP_1A and interferon γ-induced protein 10 (IP_10) were verified for IA, uIA and SAH, respectively. In the reverse Mendelian randomization analysis, the common cytokines altered by uIA and SAH were vascular endothelial growth factor (VEGF), MIP_1A, IL_9, IL_10 and IL_17, respectively. The meta-analysis results show that MIP_1A and IP_10 could be associated with the decreased risk of IA, and MIP_1A and IP_10 were associated with the decreased risk of uIA and SAH, respectively. Notably, the levels of VEGF, MIP_1A, IL_9, IL_10 and TNF_A were increased with uIA. Comprehensive heterogeneity and pleiotropy analyses confirmed the robustness of these results. CONCLUSION: Our study unveils a bidirectional association between inflammatory cytokines and IA, uIA and SAH. Further investigations are essential to validate their relationship and elucidate the underlying mechanisms.

Single-cell RNA-seq reveals novel interaction between muscle satellite cells and fibro-adipogenic progenitors mediated with FGF7 signalling.

BACKGROUND: Muscle satellite cells (MuSCs) exert essential roles in skeletal muscle adaptation to growth, injury and ageing, and their functions are extensively modulated by microenvironmental factors. However, the current knowledge about the interaction of MuSCs with niche cells is quite limited. METHODS: A 10× single-cell RNA sequencing (scRNA-seq) was performed on porcine longissimus dorsi and soleus (SOL) muscles to generate a single-cell transcriptomic dataset of myogenic cells and other cell types. Sophisticated bioinformatic analyses, including unsupervised clustering analysis, marker gene, gene set variation analysis (GSVA), AUCell, pseudotime analysis and RNA velocity analysis, were performed to explore the heterogeneity of myogenic cells. CellChat analysis was used to demonstrate cell-cell communications across myogenic cell subpopulations and niche cells, especially fibro-adipogenic progenitors (FAPs). Integrated analysis with human and mice datasets was performed to verify the expression of FGF7 across diverse species. The role of FGF7 on MuSC proliferation was evaluated through administering recombinant FGF7 to porcine MuSCs, C2C12, cardiotoxin (CTX)-injured muscle and d-galactose ( d-gal)-induced ageing model. RESULTS: ScRNA-seq totally figured out five cell types including myo-lineage cells and FAPs, and myo-lineage cells were further classified into six subpopulations, termed as RCN3+, S100A4+, ID3+, cycling (MKI67+), MYF6+ and MYMK+ satellite cells, respectively. There was a higher proportion of cycling and MYF6+ cells in the SOL population. CellChat analysis uncovered a particular impact of FAPs on myogenic cells mediated by FGF7, which was relatively highly expressed in SOL samples. Administration of FGF7 (10 ng/mL) significantly increased the proportion of EdU+ porcine MuSCs and C2C12 by 4.03 ± 0.81% (P < 0.01) and 6.87 ± 2.17% (P < 0.05), respectively, and knockdown of FGFR2 dramatically abolished the pro-proliferating effects (P < 0.05). In CTX-injured muscle, FGF7 significantly increased the ratio of EdU+/Pax7+ cells by 15.68 ± 5.45% (P < 0.05) and elevated the number of eMyHC+ regenerating myofibres by 19.7 ± 4.25% (P < 0.01). Under d-gal stimuli, FGF7 significantly reduced γH2AX+ cells by 17.19 ± 3.05% (P < 0.01) in porcine MuSCs, induced EdU+ cells by 4.34 ± 1.54% (P < 0.05) in C2C12, and restored myofibre size loss and running exhaustion in vivo (all P < 0.05). CONCLUSIONS: Our scRNA-seq reveals a novel interaction between muscle FAPs and satellite cells mediated by FGF7-FGFR2. Exogenous FGF7 augments the proliferation of satellite cells and thus benefits muscle regeneration and counteracts age-related myopathy.

Hematocrit drift and outcomes in surgical patients with aneurysmal subarachnoid hemorrhage.

BACKGROUND: There is a paucity of conclusive evidence regarding the impact of downward drift in hematocrit levels among patients who have undergone surgical clipping for aneurysmal subarachnoid hemorrhage (aSAH). This study endeavors to explore the potential association between hematocrit drift and mortality in this specific patient population. METHODS: A cohort study was conducted, encompassing adult patients diagnosed with aSAH at a university hospital. The primary endpoint was follow-up mortality. Propensity score matching was employed to align patients based on their baseline characteristics. Discrimination capacity across various models was assessed and compared using net reclassification improvement (NRI). RESULTS: Among the 671 patients with aSAH in the study period, 118 patients (17.6%) experienced an in-hospital hematocrit drift of more than 25%. Following adjustment with multivariate regression analysis, patients with elevated hematocrit drift demonstrated significantly increased odds of mortality (aOR: 2.12, 95% CI: 1.14 to 3.97; P = 0.019). Matching analysis yielded similar results (aOR: 2.07, 95% CI: 1.05 to 4.10; P = 0.036). The inclusion of hematocrit drift significantly improved the NRI (P < 0.0001) for mortality prediction. When in-hospital hematocrit drift was served as a continuous variable, each 10% increase in hematocrit drift corresponded to an adjusted odds ratio of 1.31 (95% CI 1.08-1.61; P = 0.008) for mortality. CONCLUSIONS: In conclusion, the findings from this comprehensive cohort study indicate that a downward hematocrit drift exceeding 25% independently predicts mortality in surgical patients with aSAH. These findings underscore the significance of monitoring hematocrit and managing anemia in this patient population.