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Aims To explore the knowledge, attitudes and practice status of the intrahospital transport (IHT) of critically ill patients among clinical nurses and their influencing factors. Design Cross‐sectional study. Methods A questionnaire determined the nurses' knowledge, attitudes and practice scores. The questionnaire was used for data collection in a tertiary hospital from 10 January to 17 January 2023. Multivariate regression analysis was also used to evaluate the related factors of IHT of critically ill patients in different dimensions. Results Out of 670 distributed questionnaires, 612 nurses returned the completed questionnaire. The scores of KAP were (9.72 ± 1.61), (42.91 ± 4.58) and (82.84 ± 1.61), respectively. Pearson's correlation analysis showed that knowledge, attitude and behaviour scores were positively correlated. Variables that were associated with the scores of transfer knowledge were the scores of transfer practice, different departments and the scores of transfer attitude. The score of practice, number of IHT and received hospital‐level training had statistical significance on the nurses' attitude scores. Furthermore, the score of the attitude and transport knowledge had statistical significance on the nurses' practice. Conclusion The findings indicate a clear need for clinical nurses' knowledge of IHT of critically ill patients, especially in the emergency department (ED) and ICU. In addition, nurses need to be more active in transporting critically ill patients. Managers should enhance nurses' confidence in the IHT of critically ill patients and promote clinical nurses to establish a correct and positive attitude. Impact The findings of this study benefit nursing managers in understanding the current situation of IHT of critically ill patients. Managers should apply new training methods to nursing education and develop a multi‐level training program that is systematic, comprehensive and demand‐oriented. Patient or Public Contribution The participants of this study were nurses and this contribution has been explained in the Data collection section. There was no patient contribution in this study.

Background Chinese government launched a pilot study on public long-term care insurance (LTCI) recently. Guangzhou is one of the fifteen pilot cities, officially started providing LTCI in August 2017. An in-depth analysis of experimental data from the pilot city may provide suggestions for developing a fair and effective LTCI system. This study aimed to evaluate the LTCI pilot by exploring the characteristics and care needs of claimants, and performance of the assessment tool. Methods A retrospective cross-sectional study in which claims data between July 2018 and March 2019 in the Guangzhou pilot was analyzed. LTCI claimants during the study period were included. The care needs were determined based on claimants’ physical function assessed by the Barthel Index and their medical conditions. Rasch analysis was used to explore the performance of the Barthel Index. Results Among 4810 claimants included, 4582 (95.3%) obtained LTCI benefits. Of these beneficiaries, 4357 (95.1%) were ≧ 60 years old, and 791 (17.3%) had dementia. Among 228 (4.7%) unsuccessful claimants, 22 (0.5%) had dementia. The prevalence of stroke was high in beneficiaries with (38.1%) or without dementia (56.6%), as well as in unsuccessful claimants with (40.9%) or without dementia (52.4%). Beneficiaries without dementia needed more support for basic activities of daily living and nursing care than those with dementia, while beneficiaries with dementia were more likely to be institutionalized. Five (22.7%) unsuccessful claimants with dementia and 48 (23.3%) unsuccessful claimants without dementia were disabled in at least two basic self-care activities. Regarding Barthel Index, Rasch analysis showed threshold disordering in “mobility” and “climbing stairs”, and the narrow interval was observed between all the adjacent categories of the ten items (< 1.4 logits). Conclusions Stroke and dementia were two common reasons for needing long-term care in LTCI claimants. The Barthel Index is not suitable for assessing and dividing LTCI claimants, because of inappropriate items and narrow category responses. A comprehensive assessment and grading system is required, together with needs-led care services. The eligibility should be expanded gradually based on balance finance solutions.

Posttranslational modification (PTM) of the amyloid precursor protein (APP) plays a critical role in Alzheimer’s disease (AD). Recent evidence reveals that lactylation modification, as a novel PTM, is implicated in the occurrence and development of AD. However, whether and how APP lactylation contributes to both the pathogenesis and cognitive function in AD remains unknown. Here, we observed a reduction in APP lactylation in AD patients and AD model mice and cells. Proteomic mass spectrometry analysis further identified lysine 612 (APP-K612la) as a crucial site for APP lactylation, influencing APP amyloidogenic processing. A lactyl-mimicking mutant (APP K612T ) reduced amyloid-β peptide (Aβ) generation and slowed down cognitive deficits in vivo. Mechanistically, APP K612T appeared to facilitate APP trafficking and metabolism. However, lactylated APP entering the endosome inhibited its binding to BACE1, suppressing subsequent cleavage. Instead, it promoted protein interaction between APP and CD2-associated protein (CD2AP), thereby accelerating the endosomal-lysosomal degradation pathway of APP. In the APP23/PS45 double-transgenic mouse model of AD, APP-Kla was susceptible to L-lactate regulation, which reduced Aβ pathology and repaired spatial learning and memory deficits. Thus, these findings suggest that targeting APP lactylation may be a promising therapeutic strategy for AD in humans.

Sleep is a crucial aspect of geriatric assessment for hospitalized older adults, and implementing AI-driven technology for sleep monitoring can significantly enhance the rehabilitation process. Sleepsense, an AI-driven sleep-tracking device, provides real-time data and insights, enabling healthcare professionals to tailor interventions and improve sleep quality. This study explores the perspectives of an interdisciplinary hospital team on implementing Sleepsense in geriatric hospital care. Using the interpretive description approach, we conducted focus groups with physicians, nurses, care aides, and an activity worker. The Consolidated Framework for Implementation Research (CFIR) informed our thematic analysis to identify barriers and facilitators to implementation. Among 27 healthcare staff, predominantly female (88.89%) and Asian (74.1%) and mostly aged 30–50 years, themes emerged that Sleepsense is perceived as a timesaving and data-driven tool that enhances patient monitoring and assessment. However, barriers such as resistance to change and concerns about trusting the device for patient comfort and safety were noted, while facilitators included training and staff engagement. The CFIR framework proved useful for analyzing implementation barriers and facilitators, suggesting future research should prioritize effective strategies for interdisciplinary team support to enhance innovation adoption and patient outcomes in rehabilitation settings.

Background The nucleotide-binding oligomeric domain (NOD)-like receptor protein 3 (NLRP3) inflammasome is believed to be a key mediator of neuroinflammation and subsequent secondary brain injury induced by ischemic stroke. However, the role and underlying mechanism of the NLRP3 inflammasome in neonates with hypoxic-ischemic encephalopathy (HIE) are still unclear. Methods The protein expressions of the NLRP3 inflammasome including NLRP3, cysteinyl aspartate specific proteinase-1 (caspase-1) and interleukin-1β (IL-1β), the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionicacid receptor (AMPAR) subunit, and the ATPase valosin-containing protein (VCP/p97), were determined by Western blotting. The interaction between p97 and AMPA glutamate receptor 1 (GluA1) was determined by co-immunoprecipitation. The histopathological level of hypoxic-ischemic brain damage (HIBD) was determined by triphenyltetrazolium chloride (TTC) staining. Polymerase chain reaction (PCR) and Western blotting were used to confirm the genotype of the knockout mice. Motor functions, including myodynamia and coordination, were evaluated by using grasping and rotarod tests. Hippocampus-dependent spatial cognitive function was measured by using the Morris-water maze (MWM). Results We reported that the NLRP3 inflammasome signaling pathway, such as NLRP3, caspase-1 and IL-1β, was activated in rats with HIBD and oxygen-glucose deprivation (OGD)-treated cultured primary neurons. Further studies showed that the protein level of the AMPAR GluA1 subunit on the hippocampal postsynaptic membrane was significantly decreased in rats with HIBD, and it could be restored to control levels after treatment with the specific caspase-1 inhibitor AC-YVAD-CMK. Similarly, in vitro studies showed that OGD reduced GluA1 protein levels on the plasma membrane in cultured primary neurons, whereas AC-YVAD-CMK treatment restored this reduction. Importantly, we showed that OGD treatment obviously enhanced the interaction between p97 and GluA1, while AC-YVAD-CMK treatment promoted the dissociation of p97 from the GluA1 complex and consequently facilitated the localization of GluA1 on the plasma membrane of cultured primary neurons. Finally, we reported that the deficits in motor function, learning and memory in animals with HIBD, were ameliorated by pharmacological intervention or genetic ablation of caspase-1. Conclusion Inhibiting the NLRP3 inflammasome signaling pathway promotes neurological recovery in animals with HIBD by increasing p97-mediated surface GluA1 expression, thereby providing new insight into HIE therapy.

Precisely quantifying the spatiotemporal variation patterns of ecosystem water use efficiency (WUE) (i.e., WUE and WUE ) and carbon use efficiency (CUE) across diverse regions, as well as identifying the spatial heterogeneity of their principal influencing factors, are crucial for elucidating the complex underlying mechanisms governing carbon and water cycles in the Yellow River Basin (YRB). In this study, we utilized multi-source remote sensing data, and employed Ensemble Empirical Mode Decomposition (EEMD) to explore the nonlinear spatiotemporal trends and patterns of WUE , WUE , and CUE within the YRB ecosystem. Additionally, we applied the optimally parameterized XGBoost and SHAP models to discern the spatial heterogeneity of the key factors driving their spatiotemporal variations. The results showed that: (1) The WUE , WUE , and CUE of the YRB ecosystem exhibited a spatial distribution pattern characterized by higher values in the southeast and lower values in the northwest, with these metrics were predominantly concentrated at elevations ranging from 1000 to 1500 meters. (2) The interannual change rates of the yearly average values of WUE , WUE and CUE in the YRB ecosystem were 0.008 , 0.005 , and 0.001, respectively. The predominant change patterns for WUE and WUE were monotonic increases, covering approximately 42.44% and 41.97% of the watershed area, respectively. In contrast, the change pattern for CUE was primarily a decrease followed by an increase, observed across 42.51% of the watershed area. (3) In the YRB ecosystem, the leaf area index (LAI) emerged as the primary determinant of WUE and WUE . Specifically, WUE and WUE both showed an upward trend in tandem with the increase in LAI. Furthermore, temperature was identified as the key driving factor for CUE within the YRB ecosystem. (4) In the YRB ecosystem, LAI exhibited the highest importance index for both WUE and WUE . It played a dominant role in approximately 42.80% and 45.35% of the study areas for WUE and WUE , respectively. Conversely, temperature was a crucial factor influencing the spatial variability of CUE in the YRB ecosystem, exerting a predominant influence in 38.88% of the study areas.

Understanding the spatiotemporal patterns of cropland carbon and carbon water use efficiency (CWUE) and its driving factors is essential for sustainable agricultural development. Based on a multi-source remote sensing dataset, this study applies a trend analysis (Sen + Mann–Kendall), a dual-type randomized extraction algorithm, and an optimized XGBoost model to examine the spatiotemporal variations in cropland CWUE, including the water use efficiency of net primary production (WUENPP), water use efficiency of gross primary production (WUEGPP), and carbon use efficiency (CUE) in Henan Province from 2001 to 2019. This study further quantifies the impact of irrigation on the cropland CWUE and explores the synergistic effects of its driving factors in irrigated areas. Results reveal significant regional differences in cropland CWUE across Henan Province. Higher multi-year average values of CUE and WUENPP were observed in the western region, while the WUEGPP was more prominent in the south-central region. Over 76% of cropland areas showed a general downward trend in three indicators, with significant interannual declines. Non-irrigated cropland exhibited higher CWUE values than irrigated ones. The average values over multiple years of the WUEGPP, WUENPP, and CUE of irrigated cropland were 2.51 g C m−2 mm−1, 1.08 g C m−2 mm−1, and 0.43, respectively. Sunlight was the dominant factor influencing the WUEGPP in irrigated areas, while precipitation primarily regulated the WUENPP and CUE. The influence of the gross domestic product (GDP) was found to be minimal. Notably, both the leaf area index (LAI) and precipitation exhibited a shift from a positive to negative influence on CUE once their values exceeded optimal thresholds, indicating that resource overabundance can lead to physiological limitations. This study offers valuable insights into how irrigated cropland responds to the combined effects of multiple environmental and socio-economic drivers.

Monocyte-derived dendritic cells (moDC) are an important scientific and clinical source of functional dendritic cells (DC). However, the optimization of the generation process has to date mainly been limited to the variation of soluble factors. In this study, we investigated the impact of the cell culture dish surface on phenotype and cytokine profile. We compared a standard cell culture dish to a non-adherent culture dish for two immunogenic maturation conditions, two tolerogenic conditions, and an unstimulated control. Phenotype, cytokine profile and T cell stimulatory capacity were determined after a 3-day culture. Light microscopy revealed an increase in homotypic cluster formation correlated with the use of non-adherent surfaces, which could be reduced by using blocking antibodies against CD18. All surface markers analyzed showed moderate to strong differences depending on the culture dish surface, including significantly decreased expression of key maturation markers such as CD80, CD86, and CCR7 as well as PD-L1 on cells stimulated with the Jonuleit cytokine cocktail cultured on a non-adherent surface. Significant differences in the secretion of many cytokines were observed, especially for cells stimulated with LPS, with over 10-fold decreased secretion of IL-10, IL12-p40, and TNF-α from the cells cultured on the non-adherent surface. All immunogenic moDC populations showed similar capacity to induce antigen-specific T cells. These results provide evidence that the DC phenotype depends on the surface used during moDC generation. This has important implications for the optimization of DC-based immunotherapy development and underlines that the local surrounding can interfere with the final DC population beyond the soluble factors.

Background To assess the safety and efficacy of dabigatran-based triple antithrombotic (TAT) regimen in patients after percutaneous coronary intervention (PCI) with atrial fibrillation (AF). Methods A multicenter, open-label, randomized controlled trial across 50 Chinese hospitals enrolled nonvalvular AF patients after coronary stenting. Participants were randomly assigned to receive dabigatran (110 mg twice/daily) or warfarin-based TAT regimen (dabigatran or warfarin with aspirin and clopidogrel) for 1 month and then convert to dual antithrombotic therapy (dabigatran or warfarin with clopidogrel) for 6 months. The primary safety endpoint was the first occurrence of clinically relevant bleeding (BARC types 2–5). Secondary endpoints included net adverse clinical events (NACEs) and major or clinically relevant non-major bleeding (CRNB). And the efficacy endpoint was the major adverse cardiac and cerebral events (MACCEs). Results The study was terminated early due to COVID-19 impacting recruitment. A total of 540 patients were enrolled. BARC types 2–5 bleeding occurred in 8.0% and 4.3% of patients in warfarin and dabigatran groups, respectively (HR 0.54; 95% CI 0.26–1.09; P  = 0.0861). And total bleeding events (BARC 1–5) were 20.5% and 9.4% (HR 0.44; 95% CI 0.27–0.70; P  = 0.0005). Dabigatran showed a lower total bleeding risk than warfarin, with similar risks for BARC types 2–5 bleeding, NACEs, CRNB, major bleeding, and MACCEs. Conclusions Among AF patients underwent PCI, the dabigatran-based TAT regimen did not significantly reduce the rate of BARC types 2–5 bleeding at 6 months compared with warfarin-based regimen, although the power of the study to find a difference was low due to early termination (COACH-PCI, NCT03536611, https://clinicaltrials.gov/show/NCT03536611 ).

Posttranslational modification (???) of the amyloid precursor protein (APP) plays a critical role in Alzheimer's disease (AD). Recent evidence reveals that lactylation modification, as a novel PTM, is implicated in the occurrence and development of AD. However, whether and how APP lactylation contributes to both the pathogenesis and cognitive function in AD remains unknown. Here, we observed a reduction in APP lactylation in AD patients and AD model mice and cells. Proteomic mass spectrometry analysis further identified lysine 612 (APP-K612la) as a crucial site for APP lactylation, influencing APP amyloidogenic processing. A lactyl-mimicking mutant (APP, ) reduced amyloid-B peptide (Ap) generation and slowed down K612T cognitive deficits in vivo. Mechanistically, APP eur appeared to facilitate APP trafficking and metabolism. However, lactylated APP entering the endosome inhibited its binding to BACE1, suppressing subsequent cleavage. Instead, it promoted protein interaction between APP and CD2-associated protein (CD2AP), thereby accelerating the endosomal-lysosomal degradation pathway of APP. In the APP23/PS45 double-transgenic mouse model of AD, APP-Kla was susceptible to L-lactate regulation, which reduced Ap pathology and repaired spatial learning and memory deficits. Thus, these findings suggest that targeting APP lactylation may be a promising therapeutic strategy for AD in humans.