Mineral scaling, driven by concentration polarization, is an inevitable challenge in electro-membrane technologies for recovering valuable metals from lithium-ion battery (LIB) leachates. Here, we elucidate the synergistic scaling mechanism and propose an electric field-assisted organic acid control (eF-OAC) principle to prevent membrane mineral scaling while enabling metal recovery. The eF-OAC utilizes an electric field to direct organic acids into the membrane matrix, where ligand-metal coordination dissolves hydroxide-rich scale and mobilizes metal species for selective transport and crystallization. Dynamic experimental analysis reveals that concentration polarization enriches metal hydroxides at the membrane interfaces and pores. Static density functional theory calculations further demonstrate that organic ligands are thermodynamically favored over sulfonate groups for coordinating metal hydroxides, enabling targeted dissolution from the membrane. Leveraging this molecular-level selectivity, the eF-OAC converts scale into recoverable crystalline products. In optimized electro-membrane crystallization, this eF-OAC achieves high recovery rates of 97.6% for Li+, 95.3% for Ni2+, 94.2% for Co2+, and 97.8% for Mn2+. It further yields high-purity Li2SO4 (99.4%), Ni(OH)2 (99.2%), Co(OH)2 (99.0%), and Mn3O4 (99.3%). This study clarifies the mechanisms of mineral scaling and demonstrates a scaling-free approach that transforms fouling liabilities into valuable resource recovery for spent LIBs.
This paper explores the uniqueness of Canadian Roman Catholic healthcare organizations from theological, strategic, and operational perspectives. By arguing that Canadian Roman Catholic healthcare understands that suffering is inevitable for all people at some point in their lives, the paper indicates that patient and family accompaniment through their experiences of suffering is one of the unique dimensions of a Roman Catholic ethos of care. The paper draws upon concepts and ideas from various traditional Christian sources to articulate a robust theology that can guide the building of this ethos in organizational contexts. Consideration is then given to how this theology can be operationalized, first from a strategic leadership vantagepoint, then within the context of a concrete proposal for palliative care.
India's health system is at a crossroads. With its population suffering from the dual challenges of chronic non-communicable diseases and endemic infectious diseases, the time is apt for adopting an integral, equitable, and participatory healthcare model. Family medicine, based on principles of continuity, completeness, and community orientation, presents one promising answer. Internationally, family physicians have demonstrated the ability to bridge the gap between clinical care and public health outcomes. Though. Family medicine has been misunderstood in India and treated as general practice in the absence of proper institutional support and education. However, momentum is gaining. Initiatives by the government such as Ayushman Bharat Health and Wellness Centres are evidence of intensifying efforts towards robust primary care. National endeavours for primary care conferences such as FMPC-2024 are stimulating the countrywide discussion and converging different stakeholders. Family physicians are increasingly recognised not only as clinicians but also as teachers, public health partners, and system leaders. In order to really fortify India's health system, reshaping medical training so that generalist care is prioritised, incentivising rural work, and informing the public of the essential contributions of family physicians is inevitable. Consequently, needs investment in research, digital health, and gender-sensitive policy. In the end, family medicine is the way toward equity, efficiency, and compassion. It bridges the gap between the individual and the population. For as dynamic and pluralistic as India is, it is the long-term path towards healthier living and resilient communities.
Collagen fibers are commonly used as raw materials for artificial collagen casings/films. Due to the inevitable disruption and reorganization during the processing, the re-prepared films have poorer performances, especially in mechanical properties. This study aims to explore the effects of different sourced hydrocolloids on the film-forming properties of collagen fibers, and also to evaluate the application effects on chilled meat preservation. Different hydrocolloids had various abilities to reduce the viscosity and modulus of collagen fiber dispersions. They improved the mechanical properties of the collagen fiber films, with two proteins (gelatin and soy protein isolate) showing more significant performance in dry tensile strength, while two polysaccharides (chitosan and corn starch) performed better in wet tensile strength. Chitosan and corn starch reduced the swelling ratio of the composite films, relating to their better wet mechanical properties. Different hydrocolloids also enhanced the thermodynamic stability of the films, with gelatin having the most significant effect. The addition of hydrocolloids did not significantly affect the structural integrity of collagen and they promoted the unfolding of collagen fiber bundles to a certain extent. Different hydrocolloids improved the preservation effect of composite films on chilled meat, with two polysaccharide substances having a more significant impact. This study analyzed the effects and mechanisms of different sourced hydrocolloids in the fabrication of collagen fiber film. They improved the performances of films to varying degrees and enhanced the preservation effect of chilled meat. This research could provide insights for the use of hydrocolloids in collagen fiber film systems. © 2026 Society of Chemical Industry.
Aging is an inevitable and progressive process associated with declines in physical fitness and impairments in both static and dynamic balance. Although previous studies have investigated individual components of physical fitness and balance separately, the relationships between comprehensive physical fitness measures and distinct aspects of balance in older adults remain unclear. Therefore, this study aimed to investigate the relationships between physical fitness levels and static and dynamic balance in older adults, thereby contributing to the development of more targeted assessment and rehabilitation strategies. This cross-sectional observational study used correlation analyses to examine the associations between physical fitness and balance outcomes in older adults. Given the exploratory nature of the analyses and the absence of correction for multiple comparisons, the findings should be interpreted with caution. This cross-sectional observational study examined 153 community-dwelling older adults (52.9% female and 47.1% male) aged 65 years and over who were attending the Geriatrics Outpatient Clinic at the Inönü University Turgut Özal Medical Centre in Malatya, Turkey. Physical fitness was assessed using the Senior Fitness Test, while static balance was evaluated using the One-Leg Stance Test, and dynamic balance was evaluated using the Functional Reach Test and the Timed Up and Go Test. Correlation analyses were performed to examine the relationships between the various components of physical fitness and the different balance outcomes. A statistically significant relationship was found between dynamic balance (as measured by the functional reach test) and the 6-minute walk test, the chair stand test and the arm curl test, with correlation coefficients ranging from weak to moderate (r = 0.32 to 0.46). Similarly, weak-to-moderate negative associations were observed between the Timed Up and Go test and the 6-minute walk and back scratch tests (r = - 0.30 to - 0.31). Tests measuring the physical fitness level of older individuals were associated with dynamic balance level, while no association was found with static balance level.
Accurate estimation of State of Charge (SOC) and State of Health (SOH) is critical for safe and reliable operation of lithium-ion batteries under temperature variations and long-term aging. Most existing approaches estimate SOC and SOH independently using separate models validated under limited thermal conditions, restricting practical applicability. This paper argues that battery aging through a single solid-electrolyte interphase (SEI) growth mechanism physically couples all equivalent circuit model (ECM) parameters including [Formula: see text], [Formula: see text], [Formula: see text], and OCV making multicollinearity among these features structurally inevitable, and therefore requiring a linear decorrelation stage as a necessary architectural constraint preceding any nonlinear regressor. Motivated by this argument, a PCA-enhanced XGBoost hybrid framework is proposed for simultaneous SOC and SOH estimation using task-appropriate input features. For SOC estimation, cycle number (n) and ambient temperature (T) are polynomially expanded to five dimensions [Formula: see text], z-score normalized, and projected via PCA to a four-dimensional latent representation ([Formula: see text] components, [Formula: see text] cumulative variance retained); terminal voltage, current, and time serve exclusively as sources for Coulomb Counting SOC reference labels and do not enter the regression model. For SOH estimation, the four HPPC-derived ECM parameters ohmic resistance [Formula: see text], polarization resistance [Formula: see text], diffusion capacitance [Formula: see text], and open-circuit voltage (OCV) extracted at six cycle intervals (0, 100, 200, 300, 400, and 500 cycles) serve as direct regression inputs; these features are polynomially expanded, z-score normalized, and projected via PCA to a four-dimensional latent representation ([Formula: see text] components, [Formula: see text] cumulative variance retained), with SOH labels derived from experimentally measured discharge capacity normalized by initial cell capacity. Both tasks share the same PCA-XGBoost architectural pipeline with task-specific input feature sets, and the Variance Inflation Factor (VIF) analysis directly justifies the mandatory PCA decorrelation stage for the SOH task, where [Formula: see text] exceeds the severity threshold at cycle 200 ([Formula: see text]), confirming that passing raw ECM features into any regressor without prior decorrelation would produce unstable predictions. The framework is validated on a [Formula: see text] NMC cell discharged under five temperatures ([Formula: see text] to [Formula: see text]) for SOC estimation and cycled over 500 charge-discharge cycles at [Formula: see text] for SOH estimation. Comparative evaluation against nine machine learning models achieves minimum RMSE values of 0.00871 for SOC and 0.00847 for SOH, with pack-level scalability confirmed through a [Formula: see text] simulation study (test [Formula: see text]).
Sleep deprivation (SD), together with inevitable stress inherent to conventional SD protocols, can induce oxidative stress and inflammation, thereby increasing the risk of premature death. However, the source and signaling pathways underlying reactive oxygen species (ROS) generation remain unclear. Here, we demonstrate that both mechanical and thermogenetic SD, along with possible stress induced by both protocols, lead to initial ROS accumulation in Drosophila gut subregions, including the proventriculus (PV) and PV-resident hemocytes, via upregulation of dopamine (DA) biosynthesis. Intriguingly, DA acts unconventionally by activating mitochondrial reverse electron transfer (RET), presumably through modifying interactions between the respiratory complex I proteins NDUFV1 and NDUFS3. RET-ROS elicits hemolymphatic IMD/Relish-mediated antibacterial defense. However, during chronic SD, downregulation of the Drosophila APOE/D ortholog Neural Lazarillo promotes the recruitment of hemocytes to the central brain and, together with this process, leads to widespread neuronal ROS accumulation in an Alzheimer's disease (AD) fly model. Inhibiting RET or hemocytic DA levels extends the survival of animals under chronic SD. Our work reveals DA-driven RET-ROS in innate immune cells during SD, highlights the pivotal role of a gut-innate immune-brain crosstalk in mediating the effect of SD manipulation on aging and AD pathogenesis, and suggests ways to lessen the consequence of SD, a profound health issue in modern society.
The global shift toward a service-oriented economy has made emotional labor an inevitable occupational demand, yet its impact on frontline bank employees' occupational health remains underexplored. Drawing on Conservation of Resources theory, this study investigates the relationships among emotional labor, job burnout, turnover intention, and perceived organizational support(POS), distinguishing between surface acting and deep acting. A survey was conducted among 265 frontline employees of a commercial bank in China. Surface acting was positively associated with turnover intention, while deep acting was negatively associated. Job burnout partially mediated both relationships, with mediation proportions of 53.26% and 54.90%, respectively. POS moderated these effects: high support weakened the adverse effect of surface acting on burnout and strengthened the protective effect of deep acting. This study advances COR theory by demonstrating POS's asymmetric buffering vs. amplifying mechanisms in a high-power-distance service context. Emotional labor represents a significant occupational health risk with dimension-specific pathways, and organizational support serves as a critical external resource for buffering these risks.
There are two main ways in which a mandatory vaccination policy is often defended-by accusing vaccine refusers of 'free riding', or by appealing to the 'harm principle'. In their recent book, Roland Pierik and Marcel Verweij take the latter approach-an attractive option, as they note, due to the wide acceptance of the harm principle. But in arguing that vaccine refusal should indeed be thought to constitute harm, they end up endorsing a very controversial version of the harm principle, which we should not automatically expect to secure widespread support. Steven Smith suggests that this (common) argumentative strategy amounts to free riding on the reputation of the harm principle, and is an inevitable consequence of invoking the principle as the foundation of an argument. In its most basic form, the principle is hard to resist. But in order to use it to justify a policy, you need to make some assumptions about what constitutes harm, which will lose you supporters along the way. In appealing to the wide appeal of the harm principle, Pierik and Verweij do not adequately recognise the controversial nature of their claims, and thus the need for stronger and more elaborate arguments in their support.
Worldwide, new technologies appeared to be inevitable for human being. Man is the creator of all these technologies but the core question is whether these innovations are dangerous and threatening for creativity, especially in arts. Technology significantly influences art creativity by providing new tools and mediums, such as digital painting and virtual reality, which expand the artistic possibilities. It also enhances the accessibility, allowing artists to reach wider audiences and fostering inclusivity within the art community. This relationship between art and technology isn't new, but the digital revolution has accelerated changes at an unprecedented pace, creating exciting new possibilities while challenging the traditional notions of creativity, ownership, and what we even consider "art" in the first place. While AI can enhance efficiency, it lacks the instinct, emotion, and nuance that human-driven storytelling provides. Emerging technologies such as Artificial Intelligence (AI), Virtual Reality (VR), and blockchain are re-shaping the creative industries by enabling new forms of expression, expanding access to global audiences, and redefining how art is produced, distributed, and experienced. However, if an AI creates a piece, should the credit go to the machine, the programmer, or the artist who directed it? There is a completely understandable and reasonable concern that AI-generated art may lead to homogenization, where artworks start to look similar due to reliance on the same algorithms and datasets. While the nature of the creative process is under debate, many believe that creativity relies on real-time combinations of known neural and cognitive processes. Every original work, whether it is a music or a painting, contains within it that invisible sign of inimitableness, which Benjamin called 'the aura'. A convinced suspicion of the original work, whether it be a music, novel or a painting, saves within itself that invisible sign of irreversibility dictated to the aura.
About 1.5-2 billion years ago, an endosymbiosis between aerobic α-proteobacteria and anaerobic archaeal cells generated mitochondria, i.e., organelles capable of producing oxidative energy. The bacterial genome was fundamentally reduced and a circular mitochondrial genome evolved containing mainly the genes coding for the subunits of the electron transport chain. Before the symbiotic event, there existed a virus-host co-evolution which involved the development of sensors for detecting dangerous viral DNA/RNA molecules. Endosymbiosis supplied eukaryotic cells not only with an oxidative powerhouse to allow the evolution of more complex multicellular organisms but it also meant that cells now housed an organelle which was able to generate reactive oxygen species (ROS) and to leak mitochondrial DNA (mtDNA) and double-stranded RNA (dsRNA) into the cytoplasm. There is now abundant evidence that during aging and age-related diseases mitochondria are prone to release both mtDNA and dsRNA. In the cytoplasm, mtDNA/dsRNA molecules activate a number of cytosolic nucleic acid sensors leading to the secretion of type-1 interferons (IFN) and many other cytokines which promote an age-related proinflammatory state. Currently, it is known that mtDNA can activate the cGAS-STING pathway, AIM2 inflammasomes, IFI16 receptors, and ZBP1 sensors and in addition mitochondrial dsRNA stimulates RIG-1/MDA5 signaling. Interestingly, there is abundant evidence that all these receptors are drivers of cellular senescence and inflammaging. For decades, there has been mounting evidence that mitochondria have a crucial role in the aging process. We will examine this question from the perspective of evolution and propose that mitochondrial evolution created an endogenic source for the leakage of dangerous mtDNA/dsRNA which subsequently stimulated cytosolic DNA/RNA sensors, an evolutionarily conserved viral defence mechanism. It seems that these two evolutionary events provided not only the basis for the inevitable process of aging but also ensuring the death of parental organisms.
Atrial fibrillation (AF) prevalence rises sharply with age due to two independent mechanisms. Ageing produces irreversible arrhythmogenic substrate changes through progressive fibrosis, cellular senescence and mitochondrial dysfunction, while modifiable risk factors such as obesity, hypertension, sleep apnoea, diabetes and alcohol use promote atrial remodelling through inflammatory, haemodynamic and metabolic pathways. These comorbidities accumulate with age but operate through distinct mechanisms. Late gadolinium enhancement magnetic resonance imaging now quantifies fibrosis burden, while circulating biomarkers track inflammation, fibrosis and disease activity, and these measures respond to treatment, providing objective evidence of substrate modification. Landmark trials have transformed management. Weight loss of 10% or more when maintained is associated with reduced AF burden. Structured risk-factor management may improve ablation outcomes and is associated with regression of AF type, with some patients moving from persistent back to paroxysmal patterns. These benefits occur across age groups, preventing arrhythmogenic substrate formation in younger patients and likely enabling reduction in AF burden in older adults. Collectively, this evidence positions risk-factor management as the fourth pillar of AF care and shifts AF from an inevitable consequence of ageing to a modifiable chronic disease when delivered effectively.
Breathlessness is prevalent in fibrotic-interstitial lung diseases (F-ILD) but remains underrecognised and undertreated. The purpose of this study was to examine perceptions of visibility of breathlessness among healthcare professionals experienced with managing patients with F-ILD. Four focus groups and three key-informant zoom interviews were held with 28 multinational participants from diverse practice settings and health disciplines. Using a qualitative inductive approach, themes were developed and confirmed through open coding and ongoing content analysis. The inevitability and invisibility of breathlessness in F-ILD were central and continuous throughout the three themes of the study: invisibility and visibility of breathlessness; complexity of breathlessness assessment; and becoming aware and prioritising breathlessness. Patients normalise and adapt to minimise their breathlessness. Exertional breathlessness and hypoxaemia are less understood by clinicians, friends, and family, contributing to its invisibility. Symptom assessment and management are complex and limited, reliance may be through an objective lens. There is a need for an easy-to integrate tool to assess and manage breathlessness. All participants were unprepared by their initial education to recognise or prioritise breathlessness as a symptom. Some sought specific training, most gained competency and awareness through role modelling and mentorship from experts. These healthcare professionals did not accept breathlessness as inevitable in F-ILD and urged others to not ignore it. Our study suggests perceptions of the invisibility and inevitability of breathlessness in F-ILD can change. Management of breathless patients can improve through awareness, education and training.
Administrative costs in U.S. non-profit acute care hospitals are widely reported to be high and rising, yet hospital administrators are largely exempt from the productivity measurement. We introduce the Administrative Accountability Gap (AAG), the systematic exemption of administrative functions from the cost-per-output accountability criteria imposed on every other clinical workforce category and ask whether high administrative cost is structurally inevitable or a governance issue. We develop the AAG construct through principal-agent theory and operationalize it using the formally designated Administrative and General (A&G) cost center from CMS HCRIS Worksheet A. We analyzed 6,354 non-profit hospital-year observations across fiscal years 2021-2023. We complement the empirical analysis with an illustrative management accounting framework applied to a model hospital, with sensitivity analysis. Among 2,142 non-profit acute care hospitals in FY2023, median A&G cost was 17.9% of total cost (Ranged 12.4% (10th percentile) - 25.1% (90th percentile)). Non-profit A&G share (17.9%) differed significantly from for-profit (20.3%) and government (15.4%) hospitals (p < 0.001). Using an illustrative model, we show that $0.56 M-$3.64 M in possible avoidable annual costs attributable to a single administrative domain. Administrative cost intensity varies substantially among otherwise comparable non-profit hospitals, supporting the view that it reflects governance rather than necessity. Existing management accounting tools can close the AAG; we propose a framework and a research agenda for institutional validation. The principal barrier is the structural conflict of interest that allows administrators to design the measurement systems they are exempt from.
Aging is a relentless process of gradual physio-biochemical non-reversible deterioration that significantly influences human health, leading to declining cellular function and increasing cellular damage; it is recognized as a major risk factor for atherosclerosis and cardiovascular (CV) disease (CVD), the leading cause of death worldwide. Although aging is inevitable, healthy aging is the key to well-being. Longevity is a desirable yet complex outcome influenced by a wide range of factors, including genetics, lifestyle choices, healthcare access, socio-economic conditions, and other environmental factors. The compromised efficiency of processes that counteract age-associated molecular damage affects CVD susceptibility and expedites the emergence of clinical disease. Recently recognized key resilience mechanisms related to aging may constitute new potential therapeutic targets. Geroscience focuses on the discovery and translation of methods and interventions to curtail or reverse age-related deficits that compromise quality of life for older individuals. The geroscience paradigm, increasingly acknowledged in medical specialties, renders possible the prevention of premature aging, the optimal treatment of geriatric diseases, the reduction of healthcare disparities and prejudices, and the extension of the population's health span. These important geroscience issues, including multimorbidity, frailty, tendency to frequent falls, cognitive and multisensory impairment, cardiac arrhythmias, coronary disease and heart failure, as well as undernutrition, sarcopenia and polypharmacy, are herein discussed, together with recent relevant medical advances. Emphasis is placed on boosting psychology and also on pharmacological and nonpharmacological interventions such as exercise and physical activity, healthy diets and lifestyle that target key components of aging, which might assist in both primary (geroprotection) and secondary prevention (gerotherapeutics) of CV and other diseases posing an enormous challenge in older age. The geroscience paradigm is increasingly recognized in medical specialties, enabling the prevention of premature aging, optimal management of geriatric ailments, reduction of health-care disparities and prejudices, and potential improvement of the population's health-span.
Thermophilic proteins are known for their stability and activity at elevated temperatures and hence serve as useful models for engineering enzymes with enhanced stability. The stability of these proteins is governed by both thermodynamic and kinetic factors that affect the folding-unfolding equilibrium and the rate of irreversible denaturation. Structural studies have shown that enhanced thermostability often results from multiple cooperative interactions, including improved hydrophobic packing, strengthened electrostatic interactions, and optimized hydrogen-bonding networks. Comparative studies between thermophilic and mesophilic proteins have helped to identify general mechanisms that support thermal adaptations. Mutational and protein-engineering approaches have further demonstrated the influence of specific amino acid residues or motifs on the stability through altered or modified local structural interactions. In recent years, computational approaches and machine learning methods have emerged as inevitable tools to predict protein stability. Although these approaches have improved the predictions, there still exist several limitations like limited training datasets, bias toward certain protein families, difficulties in model interpretation, etc. Therefore, combining experimental thermodynamic data, structural studies, and modern AI-based computational tools, it is possible to develop more reliable strategies to design thermostable proteins, in particular, for various industrial and biotechnological applications.
Myocardial ischemia-reperfusion (MI/R) injury remains an inevitable and severe clinical challenge during cardiac surgery, primarily characterized by mitochondrial dysfunction and robust CD4+ T cell infiltration. In this study, we investigated the therapeutic potential of the immune checkpoint molecule VSIG3 (V-set and transmembrane domain-containing protein 3) in mitigating MI/R injury. In clinical samples, ELISA-detectable VSIG3-related plasma immunoreactivity of an undefined molecular form was associated with myocardial injury and inflammation. Recombinant VSIG3 administration improved cardiac function in MI/R mice and was accompanied by lower cardiac extracellular vesicle (EV) levels, including a reduction in TOMM20⁺ mitochondrial-derived vesicle (MDV)-related signals. In vitro, VSIG3 attenuated apoptosis, enhanced antioxidant capacity, and preserved mitochondrial metabolism, accompanied by an associated increase in PI3K/Akt/mTOR phosphorylation at 3 h post-injury. Exogenous MDV supplementation partially counteracted the cytoprotective effects observed with VSIG3 treatment. In vivo, VSIG3 treatment reduced CD4+ T cell infiltration and suppressed inflammatory cytokines (TNF-α, IL-17α, IL-21) in myocardial tissue. In summary, exogenous MDVs behaved as detrimental stimuli in the present experimental settings, whereas VSIG3 treatment was accompanied by reduced MDV release, improved mitochondrial homeostasis, and suppressed T-cell activation. These findings support an association between VSIG3 treatment and MDV-related changes in MI/R injury, but do not establish MDV suppression as a necessary or sufficient mediator of VSIG3-mediated cardioprotection.
Non-small cell lung cancer (NSCLC) harboring EGFR-sensitizing mutations is typically characterized as an immunologically "cold" phenotype, exhibiting limited response to immune checkpoint inhibitors (ICIs). While EGFR tyrosine kinase inhibitors (EGFR-TKIs) represent the standard of care, acquired resistance is inevitable. Herein, we report a case of advanced NSCLC with an EGFR exon 19 deletion (19del). Following progression on multiple lines of TKI therapy and chemotherapy, the patient achieved a progression-free survival (PFS) of 8 months and an overall survival (OS) of 16 months upon receiving a PD-L1 inhibitor-based combination immunotherapy. To elucidate the mechanisms underlying this unexpected clinical benefit, multiplex immunofluorescence (mIF) analysis was performed on serial biopsy specimens obtained pre-immunotherapy (post-osimertinib progression) and post-immunotherapy progression. Results demonstrated that despite low PD-L1 expression in the pre-immunotherapy "responsive" specimen, the tumor immune microenvironment (TIME) exhibited a highly "inflamed" profile, characterized by high-density infiltration of T cells and B cells, as well as the formation of mature tertiary lymphoid structures (TLS). Notably, these TLS structures were virtually absent in the post-progression specimen. These preliminary, single-case observations raise the hypothesis that mature TLS formation following EGFR-TKI resistance may be associated with an immunotherapy-responsive TIME in EGFR-mutation NSCLC - A feature not captured by PD-L1 expression alone. Given the inherent limitations of single-case evidence, these findings are strictly exploratory and hypothesis-generating, and merit further prospective validation in adequately powered cohort studies.
The cavernous sinus medial wall (CSMW) is a critical structure that can be resected in cavernous sinus (CS)-invading tumors. Intraoperative venous bleeding is inevitable upon entering the CS and necessitates hemostatic agents use to cease its flow. There is no literature on the fate of CS patency after such hemostasis. This study aims to address that gap. An observational study was conducted between 2018 and 2025, including patients undergoing endoscopic endonasal approach (EEA) with CSMW or transcavernous resection for CS-invading tumors. Pre- and postoperative magnetic resonance imaging (MRI) images were collected and analyzed for CS patency. Postoperative imaging was grouped into three intervals: 0 to 3, 3 to 12, and >12 months. Demographic data were analyzed to identify predictors of CS non-patency. Of the 186 patients included, postoperative CS patency was achieved in 87.1% after 3.72 months. Univariate analysis demonstrated that preoperative CS non-patency ( p  < 0.001), incomplete gross tumor resection ( p  = 0.015), meningioma diagnosis ( p  < 0.001), and previous head and neck radiation increased the postoperative CS non-patency risk. Multivariate analysis identified preoperative CS non-patency as the only independent factor for postoperative CS non-patency (odds ratio = 9.8, p  < 0.001). Persistent non-patency at 3 and 12 months increased long-term postoperative CS non-patency risk by 5.86 and 14.7 times, respectively. This is the first study to report that postoperative CS patency is preserved in most cases after EEA requiring CSMW. A strong predictor of postoperative CS non-patency was identified as preoperative CS non-patency. Further studies are warranted to assess if CS non-patency has significant clinical correlations.
The increasing number of employed mothers in the workforce is an inevitable trend in China. Employed mothers may stop breastfeeding due to work-related stressors. However, many mothers overcome these challenges and continue breastfeeding after returning to work. This study aimed to develop and validate a tool to understand employed mothers' experiences with continuing breastfeeding after returning to work, based on Kumpfer's Resilience Framework, in China. The study comprised three phases. Phase 1 involved item pool generation through a literature review, focus groups, and a Delphi survey, followed by pre-testing with 15 mothers to finalize the breastfeeding resilience scale (BRS) trial version. In Phase 2, the trial BRS was administered in a cross-sectional survey of employed mothers from 18 provincial-level regions of China who were recruited using purposive sampling, and valid responses from 172 participants were included in item analysis and exploratory factor analysis (EFA) to develop the provisional BRS. In Phase 3, the provisional BRS and the Connor-Davidson Resilience Scale (CD-RISC) were administered in a cross-sectional survey of employed mothers from 23 provincial-level regions of China who had returned to work, using purposive sampling. Valid responses from 200 participants were included to evaluate reliability and validity and develop the formal BRS. Reliability was examined using internal consistency and split-half coefficients. Validity was assessed through content, construct, convergent, discriminant, and criterion-related validity analyses. The formal BRS contains 24 items across five dimensions. Cronbach's α was 0.897 (95% CI: 0.875-0.916) for the overall scale, and Cronbach's α coefficients for the five dimensions ranged from 0.750 (95% CI: 0.683-0.805) to 0.875 (95% CI: 0.847-0.900). Split-half reliability was 0.787. EFA yielded five factors explaining 63.139% of the variance, with all item loadings exceeding 0.50. Confirmatory factor analysis (CFA) showed that most fit indices met the recommended criteria, with χ²/df = 1.654, RMSEA = 0.057, CFI = 0.923, IFI = 0.924, TLI = 0.912, although GFI = 0.860 and NFI = 0.828 were below the 0.90 cutoff. Average variance extracted (AVE) values ranged from 0.441 to 0.570, with the social dimension having an AVE of 0.441, and composite reliability (CR) values ranged from 0.755 to 0.876. Correlation coefficients among the dimensions were below 0.50, and the square roots of the AVE values for each dimension ranged from 0.663 to 0.755. Correlations between BRS dimensions and the total score on the CD-RISC criterion scale ranged from 0.410 to 0.629, all statistically significant. This study developed and validated a Breastfeeding Resilience Scale for employed mothers after returning to work. It may provide healthcare workers engaged in breastfeeding promotion with an assessment tool to identify employed mothers' intrinsic motivation and psychological resilience throughout their breastfeeding journey. Not applicable.