搜索结果：integrity

The biological function of the cell membrane is significantly affected by a disrupted lipid bilayer. Maintaining the structural integrity of the lipid bilayer is hence crucial. In this work, a series of molecular dynamics (MD) simulations were carried out by varying ethanol and glucose concentrations to investigate the counteracting effects of glucose concentration on the ethanol-stressed disorganized hydrated model lipid bilayer, 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC). Our work highlights that the ethanol's concentration-dependent disruptive role affects bilayer integrity, as evidenced by increased lateral diffusion, reduced bilayer thickness, and enhanced disorder in the structural arrangements of the lipids, including the surface curvature order parameter. We observed that the addition of glucose, to some extent, opposes such disorganization. Our investigation reveals that glucose forms substantial hydrogen bonds with lipid headgroups, thereby reducing ethanol-headgroup interaction and promoting tighter lipid packing. The minimum-distance distribution functions suggest that, while water is excluded from the lipid tail, ethanol is found all the way towards the lipid tails, and the terminal methyl groups interact significantly, causing the lipid tails to bend toward the polar regions of the bilayer. This phenomenon however was observed less in the presence of glucose. An inverse relationship between glucose concentration and translational mobility is consistently observed across all ethanol concentrations studied, while higher ethanol content facilitates glucose mobility, regardless of the glucose concentration. This suggests a complex interplay between glucose and ethanol that modulates the diffusive dynamics of the solvent and solute, affecting lipid diffusion and its structural integrity. The computation of the potential of mean force (PMF) using the umbrella sampling technique highlights that the ethanol penetration process is significantly less favored and energetically hindered in the presence of glucose; as a result, lipid diffusion is slowed down. Our findings provide insights into the molecular mechanisms and underscore the protective role of glucose in stabilizing lipid bilayers under alcohol-induced stress. The study is relevant to various pharmaceutical and biomedical applications, as well as the design of biopreservation strategies for cells and tissues.

Lectins are carbohydrate-binding proteins that recognize specific glycan patterns on cell surfaces and have been increasingly explored as analytical tools in reproductive biology. This study characterized the interaction of a lectin isolated from Abelmoschus esculentus seeds (AEL) with ovine spermatozoa and evaluated its compatibility with sperm functional parameters during short-term refrigeration. Eighteen ejaculates were diluted in a Tris-egg yolk extender supplemented with 0, 1, or 3 µg/mL AEL and stored at 5°C for 24 h. Sperm motility (CASA) and flow cytometry were used to assess plasma membrane integrity and fluidity, mitochondrial membrane potential, and reactive oxygen species production. Confocal microscopy was performed to determine the localization pattern of AEL binding. AEL labeling was predominantly restricted to the sperm midpiece region. Supplementation with AEL at the tested concentrations did not affect motility patterns, membrane integrity, mitochondrial membrane potential, or ROS levels after 24 h of storage (p > 0.05). These findings indicate that AEL exhibits a consistent midpiece-associated binding pattern and does not compromise sperm functional parameters under refrigerated conditions. The results support the use of AEL as a compatible probe for investigating glycan distribution in the midpiece region of ram spermatozoa.

Intestinal barrier dysfunction is a key driver of septic liver injury (SLI). Dachaihu decoction (DCHD), a classic traditional Chinese medicine formula recorded in the Treatise on Cold Damage, is widely used to treat gastrointestinal and hepatic inflammatory conditions. The primary objective of our research was to elucidate the protective effects of DCHD against SLI and the underlying molecular mechanisms. In a murine model of sepsis induced by cecal ligation and puncture (CLP), we evaluated the therapeutic effects of DCHD on SLI by assessing serum liver enzymes, histopathology, oxidative stress, hepatocyte apoptosis, and inflammatory cytokines. Intestinal barrier integrity was examined via transmission electron microscopy, serum biomarkers (D-lactate, DAO, LPS), and tight junction proteins (ZO-1, Occludin, E-cadherin). Gut microbiota composition was analyzed using 16S rRNA sequencing. Chemical profiling of DCHD was performed via UPLC-Q-TOF-MS. Integrated network pharmacology, bioinformatics, and transcriptomic analyses identified the NF-κB/NLRP3/Caspase-1 axis as a potential mechanism, which was validated in vivo and in LPS-stimulated immortalized mouse Kupffer cells (ImKCs). Functional involvement of TLR4 and NLRP3 was further confirmed by genetic silencing of TLR4 with siRNA and pharmacological inhibition using TAK-242 (TLR4 inhibitor) and MCC950 (NLRP3 inhibitor). DCHD treatment attenuated liver injury in CLP-induced septic mice, as evidenced by improved liver function, attenuated histopathology, reduced oxidative stress, suppressed inflammation, and decreased hepatocyte apoptosis. These hepatoprotective effects were associated with reduced intestinal permeability and enhanced barrier integrity, alongside gut microbiota remodeling characterized by enrichment of beneficial bacteria and reduced abundance of gram-negative genera (e.g., Klebsiella, Enterobacter, Proteus), leading to decreased LPS production and translocation to the liver. Integrated network pharmacology and transcriptomics revealed the NF-κB/NLRP3/Caspase-1 axis as a central mechanism, with DCHD downregulating p-p65, p-IκBα, NLRP3, ASC, and Cleaved Caspase-1 in vivo and in LPS-stimulated ImKCs. Functional validation using TLR4 siRNA and the inhibitors TAK-242 and MCC950 confirmed that DCHD might attenuate liver inflammatory injury primarily through the NF-κB/NLRP3/Caspase-1 signaling pathway. DCHD may alleviate SLI by enhancing the intestinal barrier, potentially reducing the translocation of gut-derived LPS to the liver, and subsequently inhibiting the NF-κB/NLRP3/Caspase-1 axis, highlighting its considerable translational potential for SLI therapy.

The skin is far from a passive shield; it functions as a dynamic "living barrier" whose structural and immunological integrity is paramount in preventing atopic dermatitis (AD) and the subsequent progression of the atopic march toward food allergy (FA). While prophylactic emollient therapy has emerged as a promising strategy for primary prevention, recent large-scale randomized controlled trials have yielded conflicting results. In this review, we examine the complex interplay between emollient formulations, skin barrier biology, and immune responses in the context of AD and FA prevention. We discuss the functional roles of occlusives, humectants, and barrier-replenishing lipids, highlighting how their composition, ratios, and physicochemical properties determine their effects on barrier integrity. We further evaluate the impact of additional formulation components, including food-derived ingredients, haptens, irritants, and pH, as well as external factors such as product handling and application practices, which may inadvertently promote barrier disruption and transcutaneous sensitization. Collectively, current evidence supports a shift from generalized emollient use toward a precision-based, barrier-directed approach. Optimized formulations that restore physiological lipid composition, combined with early intervention and integration of objective biomarkers, may offer a more effective strategy to prevent AD and the atopic march.

Tracheal diverticulum is frequently detected incidentally on cross-sectional imaging but may pose a significant intraoperative challenge when anticipated within or adjacent to the thyroid surgical field, particularly in close proximity to the recurrent laryngeal nerve (RLN) and during central compartment (level VI) dissection. Conventionally, surgeons use preoperative computed tomography (CT) to approximate diverticular anatomy and then rely on intraoperative experience and anatomic landmarks for dissection. Recognition is challenging because intraoperative localization relies on CT correlation and anatomic landmarks within the posterior capsular plane; limited exposure may obscure the diverticulum, and a non-aerated sac may collapse and become indistinguishable from surrounding soft tissue, increasing the risk of rupture and subsequent loss of tension with further obscured planes and potential operative-field contamination. However, a standardized intraoperative workflow to functionally localize the diverticulum (and confirm tracheal communication) before definitive posterior dissection, and to verify tracheal integrity after diverticulectomy and repair, is lacking. Here, we describe a stepwise surgical technique for planned thyroidectomy in which a cervical tracheal diverticulum has been identified preoperatively. The workflow integrates preoperative contrast-enhanced CT-based risk stratification with a ventilation-assisted functional visualization maneuver [standardized endotracheal tube (ETT) repositioning within recorded cuff-depth boundaries 'D_cuff, the ETT incisor depth at which the proximal cuff margin is visualized just distal to the vocal cords; D_cuff2, the deeper ETT incisor depth after advancement beyond the diverticular level to keep the cuff distal to the diverticular ostium'] to localize the diverticular sac at the CT-predicted region and confirm tracheal communication before definitive posterior dissection. After localization, posterior dissection proceeds with deliberate RLN identification and protection, followed by controlled diverticulectomy and submerged air-leak testing under gentle manual ventilation to verify tracheal wall integrity.

The growing burden of aging-related disease and functional decline across Europe underscores the urgent need to optimize aging trajectories rather than simply extend lifespan. Achieving this goal requires identifying modifiable determinants that shape biological, psychological, and functional aging across the life course. Satisfaction with life (SWL) is emerging as one such integrative factor, linking adaptive capacity, resilience, and long-term healthspan outcomes. In this conceptual and translational paper, we integrate evidence from geroscience, psychology, and occupational health to position SWL as both a marker and a potentially modifiable determinant of healthspan. We review biological, psychological, and social mechanisms linking SWL to aging processes, including cardiovascular and inflammatory regulation, neural and affective processing, psychological resilience and reserve, and social integration and generativity. Collectively, these pathways suggest that SWL reflects the functional integrity of adaptive systems that shape vulnerability to age-related functional decline. We further argue that occupational settings represent a uniquely powerful and scalable context for targeting SWL, given their sustained influence on behavior, stress exposure, social roles, and meaning across adulthood. Building on this framework, we discuss the Semmelweis Study, a large prospective workplace-based cohort, together with the Semmelweis-EUniWell Workplace Health Promotion Program, as an integrated model for translating geroscience-informed insights into structured interventions. Such workplace health promotion programs can target core psychological capacities-including savoring, self-regulation, creative and executive efficiency, and resilience-that are closely linked to adaptive capacity and aging-related outcomes. Finally, we discuss implications for geroscience, public health, and policy, highlighting how embedding SWL as a strategic target within workplace systems may contribute to extending healthspan, strengthening workforce sustainability, and reducing the societal burden of population aging. Conceptualizing satisfaction with life not merely as a subjective outcome but as a dimension of biological aging and adaptive resilience opens new avenues for intervention at the interface of geroscience and real-world systems.

Gallbladder perforation caused by the anatomical proximity of a liver abscess or indirect inflammatory erosion occurs in less than 3% of reported cases. This case report describes the clinical course of an 84-year-old male patient who developed sepsis secondary to gallbladder perforation caused by a liver abscess. This report, through a representative case, discusses its diagnostic challenges and management strategies to enhance clinical awareness. The patient presented with a one-day history of right upper quadrant pain and fever. No signs of acute abdominal conditions, such as gastrointestinal perforation, acute pancreatitis, acute cholangitis, or acute appendicitis, were observed on the admission abdominal computed tomography (CT) scan. Within 2 days, the condition progressed with worsening abdominal pain, high fever, and hypotension. An incidental finding on contrast-enhanced ultrasound revealed a liquefied abscess in liver segment V communicating with the gallbladder lumen, confirming the diagnosis of a liver abscess with secondary gallbladder perforation. Blood culture identified Escherichia coli, indicating sepsis progression and diagnostic delay. This course illustrates rapid deterioration from localized infection to systemic life-threatening illness with organ dysfunction. Immediate interventions included ultrasound-guided percutaneous abscess drainage and culture-directed antibiotic optimization, supported by nutritional and symptomatic care. Following treatment, the patient recovered favorably, with imaging showing reduced abscess size, restored gallbladder wall integrity on follow-up ultrasound, and no recurrence on subsequent monitoring. This case unveils a rare yet fatal complication of liver abscess perforating into the gallbladder. It serves as a critical reminder for clinicians to include this entity in the differential diagnosis when a liver abscess is adjacent to the gallbladder and systemic infection worsens. Subtle clues on contrast-enhanced CT or ultrasound, such as focal discontinuity of the gallbladder wall, are key to early identification. A staged approach centered on interventional drainage, supported by a multidisciplinary team, is central to the successful treatment of such critically ill patients.

Advancements in 3D bioprinting demand bioinks that demonstrate not only precise printability and mechanical robustness but also consistent biochemical and cellular performance. From previous iterations in our laboratory, a silk fibroin-gelatin (SF-G) bioink was conjugated with mushroom tyrosinase (MT) as the enzymatic crosslinker. However, its clinical translation was hindered by several limitations, including batch-to-batch variation in concentration and enzymatic activity, protracted gelation kinetics, and inconsistent rheological and structural characteristics. To overcome these challenges, we developed a next-generation SF-G bioink employing horseradish peroxidase (HRP) and hydrogen peroxide (H2O2) as an alternative enzymatic crosslinking system. This approach facilitated rapid and tunable crosslinking through β-sheet enhancement, yielding hydrogels with improved stiffness, shape fidelity, and resistance to enzymatic degradation. Detailed rheological analysis confirmed optimal shear-thinning behaviour and print fidelity, while reactive oxygen species (ROS) quantification ensured cytocompatibility across physiologically relevant concentrations. Human bone marrow-derived mesenchymal stem cells (hBMSCs) encapsulated within the constructs maintained high viability and demonstrated robust osteogenic and chondrogenic lineage commitment. Furthermore, supplementation with triiodothyronine (T3) and transforming growth factor-β3 (TGF-β3) augmented matrix deposition and tissue-specific morphogenesis. Notably, a 10 U HRP-H2O2 formulation emerged as the most promising candidate, offering a strategic balance of mechanical integrity, bioactivity, and reproducibility. This optimized enzymatic system paves the way for scalable and clinically viable SF-G bioinks tailored for advanced tissue engineering and regenerative medicine applications.

Triplet-triplet annihilation upconversion (TTA-UC) liposomes are of emerging interest because of their potential bioapplications in biosensing/imaging and light-driven therapeutic delivery. However, a potential challenge in vivo is their stability, since liposomes are prone to enzymatic degradation. Here, for the first time, we examine the impact of phospholipase hydrolysis on TTA-UC in liposomes. We applied a TTA-UC liposome integrating a BODIPY charge transfer sensitizer and perylene emitter pair within a DOPC membrane, that exhibits intense upconverted blue emission under green excitation. Phospholipase A2 (PLA2) enzyme was applied as the phospholipase as it is ubiquitous in the body and upregulated under a number of conditions. Surprisingly, we observed that PLA2 treatment resulted in only a relatively modest decrease in TTA-UC intensity on exposure of the liposomes to the enzyme. In the presence of imipramine, a competitive inhibitor of PLA2, or absence of Ca2+ on which phospholipase hydrolysis depends, the enzymatic action is inhibited and TTA-UC intensity is indistinguishable from that in enzyme-free solution. Ca2+-dependent enzymatic activity, drug-based inhibition and the impact of hydrolytic products on membrane packing were characterized in pore-suspended lipid bilayers, using confocal-based fluorescence lifetime imaging (FLIM), fluorescence lifetime correlation spectroscopy (FLCS), and electrochemical impedance spectroscopy (EIS). FLIM and FLCS studies show that enzymatic lipid cleavage increases lipid packing and decreases membrane fluidity without significant damage to the bilayer. Thus, we conclude that the decreased TTA-UC output is due to the increased viscosity of the membrane upon hydrolysis. Electrochemcial impedance confirms these observations, where membrane admittance decreases in response to phospholipid hydrolysis indicating tighter lipid packing of the membrane with hydrolytic products. Nanoscale imaging, using atomic force microscopy (AFM) in liquid mode at a mica-supported lipid bilayer, further confirmed that PLA2 causes phospholipid hydrolysis in the presence of Ca2+, resulting in nanoscale pore formation, whereas either in the absence of Ca2+ or with imipramine-treated PLA2, it did not induce lipid hydrolysis. Overall, our findings provide a molecular basis for understanding enzymatic action in general at a liposome bilayer model and show, for the first time, the influence of enzyme hydrolysis on TTA-UC integrity and efficiency in liposomes.

The development of efficient and durable non-precious electrocatalysts for the oxygen evolution reaction (OER) remains a critical challenge for sustainable hydrogen production via water electrolysis. In this work, a series of Ce-doped CoMn-layered double hydroxide (CM-LDH-Ce) nanosheets are synthesized through a solvothermal approach, with the Ce content systematically tuned from 0 to 15 at%. Comprehensive characterization indicates that moderate Ce doping (2.5 at%) promotes the formation of a well-defined core-shell nanoarchitecture, enlarges the electrochemically active surface area, modulates the electronic structures of Co and Mn, and introduces beneficial oxygen vacancies. These integrated structural and electronic modifications lead to exceptional OER activity in alkaline medium. The optimized CM-LDH-Ce2.5 catalyst exhibits a low overpotential of 287 mV at 10 mA cm-2, requires an overpotential of 500 mV to achieve 500 mA cm-2, shows a small Tafel slope of 87.12 mV dec-1, and demonstrates remarkable stability over 100 h of continuous operation. In contrast, excessive Ce addition (≥10 at%) disrupts the layered ordering and causes severe activity degradation. This study establishes a clear dopant-dependent relationship between structural integrity and electrocatalytic function, offering a rational design strategy for high-performance LDH-based OER electrocatalysts via controlled rare-earth engineering.

Breast conservation therapy in the setting of breast cancer has been shown to be a safe method for oncologic treatment in certain patients. However, lumpectomy and radiation have historically been associated with contour deformity, asymmetry, and suboptimal aesthetic outcomes. Oncoplastic breast reconstruction is an approach to breast-conserving surgery that includes reconstruction of partial mastectomy defects in order to minimize the deformity caused by treatment. These techniques serve to optimize breast aesthetics and symmetry in the oncologic setting and have improved patient satisfaction in the setting of breast conservation. There are several key points in the planning and execution of oncoplastic surgery as well as secondary procedures to further improve outcomes. Here, the authors present an overview of patient selection, multidisciplinary planning, and surgical technique for primary and secondary reconstruction, with a focus on specific methods of improving outcomes with autologous fat transfer. This review includes an overview of the literature focusing on patient-reported outcomes (PROs), as these play an important role in a surgeon's postoperative assessment of oncoplastic breast reconstruction. Overall, patient satisfaction is high and the oncologic integrity is preserved. Clinical cases are used to illustrate conceptual framework, pertinent anatomy of various techniques, and preoperative and postoperative comparisons.

Traditional classification of traumatic brain injury (TBI) has relied predominantly on neurological responsiveness, most notably the Glasgow Coma Scale, to stratify injury severity. While this approach has provided a common clinical language for decades, it inadequately captures the biological heterogeneity, anatomical variability, and contextual factors that shape injury trajectories and outcomes. Growing recognition of these limitations has prompted the development of multidimensional classification frameworks, including the clinical, biomarker, imaging, and modifier (CBI-M) model, designed to reflect the complex and dynamic nature of TBI. The objective is to describe a structured, implementation-science-based methodology for transitioning from traditional TBI classification to the CBI-M framework while preserving clinical continuity, data integrity, and system feasibility. We propose a phased transition methodology grounded in implementation science principles, emphasizing backward compatibility, additive integration, reproducibility, scalability, and distributed responsibility. The methodology is organized into three sequential phases: (I) mapping legacy classification elements to CBI-M domains to ensure conceptual continuity; (II) operational integration through workflow-aligned, staged adoption across the trauma care continuum; and (III) system-level embedding via electronic medical records, trauma registries, governance structures, and continuous evaluation mechanisms. Explicit attention is given to data stewardship, accountability, and longitudinal consistency. The proposed methodology provides a practical roadmap for embedding multidimensional TBI classification into routine clinical practice without disrupting existing workflows or registries. By aligning classification domains with established clinical roles and care phases, the approach minimizes documentation burden while enabling incremental adoption on the basis of institutional readiness. Governance and audit mechanisms support fidelity, comparability, and sustainability over time. Transitioning to multidimensional TBI classification requires more than conceptual validity; it demands deliberate implementation strategy. The proposed methodology offers a scalable, system-aware pathway for integrating the CBI-M framework into real-world trauma care, supporting precision-oriented classification while maintaining continuity with legacy systems. This approach provides a foundation for durable adoption, quality improvement, and future research in traumatic brain injury.

TMEM16E is a transmembrane protein that functions both as a phospholipid scramblase and a non-selective ion channel, playing a critical role in cellular ion transport and membrane dynamics. Recent studies have shown that the TMEM16E scramblase also facilitates membrane internalization through macropinocytosis. This study investigates the effects of extracellular protons on TMEM16E's scrambling activity and subsequent macropinocytosis under acidic conditions, which are particularly relevant in pathophysiological contexts such as muscular dystrophies and cancers. Our results indicate that TMEM16E-induced macropinocytosis, as evidenced by the internalization of annexin V, is significantly enhanced in acidic environments (pH 5.5). However, the overall number of macropinosomes, assessed using 70 kDa dextran, remained unchanged despite variations in extracellular pH. This suggests that TMEM16E-mediated macropinocytosis operates independently of extracellular proton concentrations. Upon extracellular acidification, both TMEM16E scrambling activity and macropinocytosis were rapidly inhibited, leading to a swift decrease in intracellular Ca2+ levels compared to physiological conditions. Notably, intracellular Ca2+ was cleared more quickly in acidic environments, indicating a regulatory role for the proton-dependent Ca2+ clearance pathways. Using wound healing and MTS assays, we demonstrated that TMEM16E expression significantly enhances cell proliferation and survival under acidic conditions. Our findings underscore the importance of TMEM16E-mediated macropinocytosis in maintaining plasma membrane integrity and promoting cell survival, highlighting its role as a crucial signaling pathway in both physiological and pathological contexts.

Current biodegradable polymers for absorbable tissue ligation clips suffer from not possessing rigidity and toughness simultaneously compared with polyoxymethylene (POM) clips. To overcome the limitations, two series of biodegradable copolymers of poly(ε-caprolactone) and poly(L-lactide) with random and block architectures were designed and synthesized. Compared with random copolymer P(CL-r-LLA), diblock copolymer PCL-b-PLLA exhibited higher crystallinity and superior mechanical strength. The copolymers with 15 mol% CL composition were selected for further study, denoted as RP15 (random) and BP15 (block). The BP15 clips achieved a closure force of 27.9 ± 1.4 N, comparable to commercial POM clips (29.0 ± 2.4 N), while also offering biodegradability. The degradation studies showed that BP15 clips degraded slowly, maintaining structural integrity and sustained closure functionality for up to two weeks, which was essential for safe tissue ligation. Subcutaneous implantation in rats further confirmed that BP15 clips exhibited favorable performances, demonstrating their potential as a promising biodegradable alternative to POM for use as an absorbable tissue ligation clip.

TMS-007 is a member of the SMTP congeners for the treatment of acute ischemic stroke. To support its preclinical study, LC-MS/MS methods for the quantification of TMS-007 in rat plasma and brain were developed. The samples were prepared by protein precipitation. A UPLC HSS T3 column (2.1 mm × 50 mm, 1.8 µm) was used to achieve chromatographic separation. An acetonitrile-water mixture containing ammonium acetate was used as the mobile phase. The methods were validated with regard to selectivity, calibration curve and lower limit of quantitation, accuracy and precision, matrix effect, extraction recovery, carryover, dilution integrity, and stability. The calibration ranges of TMS-007 in rat plasma and brain homogenate were 10.0-10 000 ng mL-1. There was no endogenous or cross interference in the biological matrices. Across these matrices, the intra- and inter-batch coefficients of variation and accuracy deviations for all QC samples met the acceptance criteria. The inter-batch coefficients of variation of the QC samples were ≤11.7% for plasma and ≤15.0% for brain. The inter-batch accuracy ranged from 97.8% to 104.1% for plasma and 97.1% to 102.3% for brain. No significant matrix effect was observed from the matrices (from 102.9% to 111.0% for plasma and from 114.3% to 118.9% for brain). The extraction recoveries of the methods at different concentrations were consistent and reproducible. For plasma, the coefficients of variation were ≤9.9%, and for brain, the coefficients of variation were ≤4.6%. The analyte was stable in different matrices under various storage conditions (room temperature for 8 h, 4 °C in the autosampler for 3 days, 3 freeze-thaw cycles and 7 days at -70 °C). The methods were successfully applied to a preclinical study in a transient middle cerebral artery occlusion rat model after single dose administration. The pharmacokinetic results of the study drug laid a foundation for its further development.

Effective management of IBD necessitates ongoing evaluation of disease activity. Molecular imaging of neutrophil elastase (NE) could address this urgent need as it mechanistically targets the early event of intestinal inflammation. In this study, based on macrocyclic peptide POL6014, [68Ga]Ga-POL6014 was developed for noninvasive assessment of colitis activity and treatment response through targeting of NE. [68Ga]Ga-POL6014 exhibited high specificity and affinity for NE with the KD of 14.81 nM and IC50 of 3.02 nM. In PET imaging, [68Ga]Ga-POL6014 could quickly visualize inflammation sites with colon uptake of 3.15 ± 0.63%ID/g and colon/muscle ratio of 4.92 ± 0.74 at 30 min p.i.. The specificity of [68Ga]Ga-POL6014 was demonstrated by the dose-response blocking studies with POL6014. Furthermore, [68Ga]Ga-POL6014 PET was used to evaluate treatment response to 5-ASA. The treatment significantly inhibited colon uptake of [68Ga]Ga-POL6014 (1.71 ± 0.21 %ID/g), accompanied by a decrease in imaging contrast (2.81 ± 0.26). Immunofluorescence revealed the preservation of mucosal barrier integrity and a remarkable decrease in NE positive cells after 5-ASA treatment. Moreover, there were good correlations between PET quantification with NE expression and DAI score, indicating the reliability of [68Ga]Ga-POL6014. Additionally, [68Ga]Ga-POL6014 was widely distributed and cleared rapidly from nonspecific organs and blood pool, and was excreted through urinary system, suggesting its favorable pharmacokinetics. In conclusion, [68Ga]Ga-POL6014 is a promising tracer that enables in vivo globally mapping of neutrophil-mediated inflammation in the entire gastrointestinal tract for early diagnosis, assessment of disease activity and evaluation of anti-inflammatory treatment response.

The encapsulation of ionic liquids (ILs) within porous silica capsules templated from a Pickering emulsion offers a powerful platform for designing efficient microreactors in biphasic systems. However, a fundamental understanding of how synthesis parameters govern the textural properties and structural integrity of the porous silica capsules remains limited. This study presents a comprehensive investigation into the sol-gel synthesis of IL-containing silica capsules, establishing crucial structure-property relationships. We demonstrate that for the study of textural properties, supercritical CO2 drying is a prerequisite for preserving the capsule's native morphology and porosity, whereas conventional ambient drying causes severe shrinkage and structural collapse due to capillary forces. Leveraging this preservation method, we show that acidic catalysis (more precisely, at pH below the isoelectric point of silica, which is pH < 2) favors the formation of highly mesoporous capsules with better structural cohesion, while basic conditions result in capsules more prone to severe fragmentation. Furthermore, optimization of the reaction temperature, time and water-to-alkoxysilane ratio is found to be essential for balancing shell growth kinetics with mechanical stability. These findings provide a rational framework for engineering robust, tailored silica capsules for advanced applications in catalysis and controlled release.

Native long-read DNA sequencing simultaneously captures genetic variants and epigenetic modifications from single molecules, but preserving molecular length and base modifications currently depends on cold-chain infrastructure that limits access to well-resourced settings. We demonstrate that ensilication, the encapsulation of DNA within silica matrices, preserves DNA at ambient temperature for 30&#xa0;days with sequencing performance equivalent to conventional&#x2009;-&#x2009;80&#xa0;&#xb0;C freezing. Across three Genome-in-a-Bottle reference genomes, ensilicated and frozen samples show no significant differences in read length (N50&#x2009;~&#x2009;8,000-11,000&#xa0;bp), variant-calling accuracy, or genome-wide CpG methylation. Single-read methylation calls benchmarked against an independent bisulfite-sequencing reference confirm that ensilication introduces no detectable bias, with per-read accuracy differing by less than 0.4% between preservation conditions. Ensilicated DNA tolerates repeated handling better than frozen samples and maintains fragment integrity under accelerated weathering. In two patients with rare genetic disorders, ambient-preserved DNA resolves a de novo variant in the segmentally duplicated GTF2I locus and detects methylation patterns consistent with KDM2A-related disorder. Ensilication enables diagnostic-quality native long-read sequencing without cold-chain infrastructure, supporting ambient storage and transport while preserving both sequence and methylation information.