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Population aging poses significant challenges for community planning. While prior research has predominantly examined older adults as passive users of green spaces, less is known about how their direct involvement in green space regeneration is translated into active aging behavior. Drawing on place attachment theory, psychological ownership theory, self-determination theory, and meaning-making perspectives, this study proposes a process-based model in which participation fosters two psychological constructs-emotional imprint on place and sense of landscape ownership-that promote active aging behavior, with meaning in life incorporated as a moderator. Survey data were collected from 433 older adults aged 60 and above residing in Chinese communities with experience in green space regeneration initiatives. Partial least squares structural equation modeling (PLS-SEM) was used to estimate the measurement and structural models, with bootstrapping (5,000 resamples) for mediation analysis and a product-indicator approach for moderation. Perceived participation in green space regeneration exerts a significant positive effect on both emotional imprint on place (&#x3b2; = 0.647, p < 0.001) and sense of landscape ownership (&#x3b2; = 0.471, p < 0.001), and emotional imprint further predicts landscape ownership (&#x3b2; = 0.367, p < 0.001). Both constructs significantly predict active aging behavior (&#x3b2; = 0.290 and &#x3b2; = 0.275, both p < 0.01) and partially mediate the participation-behavior relationship. Meaning in life exhibits a dual moderating effect: it strengthens the emotional imprint-behavior link (&#x3b2; = 0.265, p < 0.001) but attenuates the landscape ownership-behavior link (&#x3b2; = -0.375, p < 0.001). The findings reveal a shift from ownership-based motivation to meaning-driven engagement in later life. By identifying psychological pathways linking participation and behavior, this study advances a place-based psychological perspective on active aging and provides practical implications for community planning that prioritize emotional connection and meaningful engagement over infrastructural provision alone.

Flaviviruses are positive-sense RNA viruses that rely entirely on host translation machinery to express their genome, making protein synthesis a central point of vulnerability. Interferon-stimulated genes (ISGs) exploit this dependence through diverse and mechanistically distinct strategies. PKR and IFIT proteins interfere primarily with translation initiation by targeting initiation factors or cap recognition, whereas SLFN11 and SAMD9L impair elongation through codon- and tRNA-dependent mechanisms. In parallel, ZAP, SHFL, and ISG20 inhibit translation by excluding viral RNAs from ribosomes or promoting their degradation. These antiviral activities highlight that ISG-mediated restriction is often highly selective, targeting viral RNAs on features such as cap structure, nucleotide composition, codon usage, and RNA folding. As a result, translation emerges as a central interface of host-virus conflict, where subtle differences between viral and cellular mRNAs can be exploited to achieve potent antiviral effects while preserving host protein synthesis. This minireview highlights recent advances in the identification and characterization of ISGs that restrict flavivirus protein synthesis and integrates them into a unified framework based on their primary mechanism of action. Emphasizing how host defenses target multiple stages of translation provides a conceptual basis for understanding how innate immunity controls flavivirus replication and highlights viral translation as a promising target for selective antiviral strategies.

The TKF92 model of molecular evolution-a linear birth-death process for indels, with finite-state continuous-time Markov chain substitutions-is exchangeable in residue identity at every site: the generative process treats amino acids symmetrically, conditional on a single substitution rate matrix. To introduce local heterogeneity, evolutionary models are often equipped with site-class mixtures, preserving this symmetry in the sense of de Finetti: conditional on the latent class, residues are still exchangeable. In a four-step theoretical ladder, we show how long-range structure such as couplings between distant sites can also be introduced exchangeably by using a Dirichlet process to partition sites into co-evolving classes. Our first step is a thorough analysis of TKF92 to establish sufficient statistics, limiting behavior, and inferential tools. We then lift the pairwise TKF92 hidden Markov model, in the limit of small time, to a time-indexed gravestone-augmented pair stochastic context-free grammar , and from there to its phylogenetic generalisation. This framing allows trajectories to be sampled exactly by Inside-Outside recursion. The third step places a Dirichlet process over the alive sites and asks co-keyed sites to evolve under a sparse Potts interaction - an exchangeably-partitioned hidden direct-coupling model whose marginal alignment likelihood is unchanged from plain TKF92. The fourth rung of the ladder develops inference machinery: a Gibbs-Metropolis sampler that alternates alignment resamples, key-partition resamples, and stochastic parameter updates. We close several gaps along the way - exact closed-form sufficient statistics for the linear birth-death-immigration component, the resolvable L'H&#xf4;pital limit at &#x3bb; = &#x3bc; , and a closed-form M-step for a recursive generalisation of TKF92 - and we report a 1,000-family Pfam fit with K =4 site classes whose Potts atoms carry &#x223c;0.54 nats of covariation per class-pair on top of a substantial single-site substitution model. Supplementary material, including full source code for inference, may be found at https://tkfdp.net /.

Sleep is a conserved animal behavior necessary for survival. It is under tight circadian and homeostatic control, and modulated by diet. Here, we identify the amino acid transporter ANIDRA (ANID) as an important sleep regulator in Drosophila . Flies lacking ANID show decreased and poorly consolidated daytime and nighttime sleep. Contrary to wild-type controls, anid mutant flies are unable to adjust their sleep to their diet, behaving as if they were constantly on a complete diet rich in amino acids. ANID is expressed in ensheathing and cortex glia, where it inhibits mTOR activity in a diet-dependent manner. Moreover, pharmacological inhibition of mTOR attenuates the anid mutant sleep phenotypes. Interestingly, DH44-expressing brain neurons, which promote arousal and sense amino acids, are constantly active in ANID's absence. We therefore propose that ANID mediates detection of dietary amino acids by ensheathing and cortex glia to regulate the activity of arousal-promoting neurons.

Mammals rely on their senses to establish their position in space. Neural activity in the hippocampus maps position, yet how sensory signals reach the hippocampus remains poorly understood. Here we uncover the visual pathways informing spatial maps in the mouse hippocampus. Hippocampal activity in mice traversing a track in alternating periods of light and darkness revealed two distinct maps, one in light and one in dark. Surprisingly, distinct maps persisted following bilateral ablations of primary visual cortex, indicating that visual signals still reach the hippocampus. Conversely, blocking the ancestral pathway linking superior colliculus to lateral visual cortex markedly reduced the difference between light and dark maps. Thus, this conserved pathway relays visual information to the hippocampus, potentially explaining residual visual navigation in cortically blind humans.

Diaries written for patients in the intensive care unit (ICU) are widely used to promote psychological recovery. By providing a structured account, diaries may help patients reconstruct their experiences and make sense of a period marked by memory loss or confusion. Many traumatic brain injury (TBI) survivors experience impaired memory, influencing both themselves and their family caregivers (FCs). The aim of this study was to gain a deeper understanding of the impact of a nurse-written ICU diary on TBI-survivors and their FCs. Nine TBI-survivors and ten FCs were interviewed as dyads in this exploratory qualitative study. Data were analyzed inductively using the interpretive description methodology. The overarching theme "Creating a shared narrative," encompassed four themes: "Piecing the parts together," describing strategies to gather information, "Negotiating the severity of the trauma," reflecting how the diary supported mutual understanding of illness severity, "Navigating an emotional terrain," capturing the emotional complexity involved, and "Humanizing the ICU experience," highlighting how the diary acknowledged the patient as a person. For TBI-survivors, the diary helped fill memory gaps and supported understanding of illness severity. For FCs, it facilitated communication and alignment of recovery expectations. Despite emotional complexity, receiving a diary was overall a positive experience.

Characterizing genetic diversity in proso millet (Panicum miliaceum L.) is essential for crop improvement and breeding programs. This study evaluated the genetic diversity, phenotypic variation, and population structure of 46 proso millet accessions using five qualitative and twelve quantitative traits across two growing seasons (2023-2024) in northern Xinjiang. Grain color showed the highest genetic diversity index (H' = 2.064), while panicle type showed the lowest (H' = 1.383). Green panicle color (84.78%), long panicle branch length (63.04%), lateral panicle type (71.74%), and yellow grain color (86.96%) were predominant. Grain yield (Y) and grain weight per panicle (GWP) exhibited the highest coefficients of variation (15.00% and 14.61%, respectively) and substantial genetic diversity indices (Y: H' = 2.11; GWP: H' = 2.12), indicating considerable selection potential. Grain yield was significantly positively correlated with grain weight per panicle (r = 0.901, P < 0.01) and main panicle length (r = 0.863, P < 0.01). Combined analysis of variance revealed highly significant genotypic effects for all agronomic traits, while genotype &#xd7; environment interaction effects were non-significant for all traits, indicating stable genotype rankings across years. Broad-sense heritability estimates were very high for yield-related traits, with grain yield (H&#xb2; = 0.998) and grain weight per panicle (H&#xb2; = 0.996) demonstrating strong genetic control. Stepwise regression analysis identified grain weight per panicle and main panicle length as the primary yield predictors (R&#xb2; = 0.91). Principal component analysis showed PC1 and PC2 explained 70.13% of total variation, representing vegetative vigor and yield capacity, respectively. Cluster analysis identified three groups with distinct trait profiles suitable for dual-purpose breeding, early-maturing cultivar development, and forage breeding, respectively. The evaluated germplasm possesses substantial genetic diversity, providing valuable resources for breeding parent selection in northern Xinjiang proso millet improvement programs.

Vascular smooth muscle cells (VSMCs) are the predominant cell type of the tunica media and are central mediators of vascular wall integrity, governing tone, remodelling and the progression of arterial disease. Despite this, mechanobiology research has historically focused on endothelial cells, leaving VSMC-intrinsic mechanosensing comparatively unexplored. Critically, VSMC phenotypic transitions from contractile to synthetic, inflammatory, osteogenic and macrophage-like states are not merely transcriptional events but involve profound bioenergetic reprogramming, a dimension that has been largely overlooked in mechanobiology. VSMCs sense and transduce diverse mechanical stimuli including cyclic stretch, shear stress, matrix stiffness and hydrostatic pressure through specialized mechanosensors such as mechanosensitive ion channels or cell surface receptors including integrins, to orchestrate phenotypic switching and vascular remodelling. Dysregulated mechanotransduction contributes to hypertension, atherosclerosis, aneurysm formation and arterial stiffening. This review provides a unified synthesis of VSMC mechanobiology across four domains: (1) mechanical microenvironment, (2) phenotypic plasticity, (3) mechanosensing pathways and (4) emerging technologies. In parallel the review also discusses emerging technologies such as organ-on-a-chip platforms that are increasingly being used to investigate these processes. Importantly, it introduces a novel integrated framework linking VSMC mechanotransduction, metabolic reprogramming and atherogenesis, positioning VSMCs at the centre of vascular mechanobiology and identifying the mechano-metabolic signalling as a therapeutically underexplored driver of cardiovascular disease.

In-plane (IP) ultrasound-guided venipuncture is widely used for its recognized advantages, including improved needle tip identification and a shallower puncture angle, which enhances echogenicity, reduces posterior wall injury, and facilitates guidewire insertion. These benefits, however, can create a false sense of security if the inherent limitations of ultrasound imaging are not appreciated. Among these, slice thickness artefact, caused by the finite elevational thickness of the ultrasound beam, is frequently overlooked in clinical practice. This narrative review examines the mechanisms, clinical implications, and strategies to mitigate slice thickness artefact during IP venipuncture, with particular emphasis on factors influencing artefact magnitude and needle tip visualization. Slice thickness artefact projects echoes from structures outside the imaging plane onto the two-dimensional image, making the needle tip appear intraluminal while it actually lies in a parallel, off-plane trajectory. Misinterpretation may increase the risk of injury to adjacent arteries, nerves, or other critical structures and lead to inadvertent extravascular catheter placement. The magnitude of the artefact depends on imaging depth, focal zone alignment, beam divergence, and transducer design, and is particularly relevant for deep, small-caliber veins and low-frequency or handheld devices. Mitigation strategies include awareness of beam limitations, careful probe selection, optimization of depth and focal zone, dynamic probe manipulation, controlled needle advancement, backflow verification, and complementary out-of-plane confirmation. When recognized and managed appropriately, slice thickness artefact can be minimized, preserving the procedural advantages of IP guidance. Understanding ultrasound beam geometry and applying targeted technical strategies are essential to optimize needle tip visualization, procedural safety, and patient outcomes.

The plasticity of dendritic cell (DC) functional state is a major hurdle in DC therapy, yet how DCs acquire distinct states independent of ontogeny remains poorly understood. Here, we demonstrate that changes in matrix stress relaxation mechanically educate DCs to adopt distinct, persistent functional states even after the removal of mechanical cues. Stem cell-derived DCs cultured in a fast-relaxing environment exhibited enhanced antigen presentation, faster migration, and higher expression of T cell-recruiting chemokines. Slow-relaxing DCs, biased towards pro-inflammatory cytokine secretion, were enriched for gene signatures associated with lipid accumulation and stress response. These mechanical responses were conserved across human and murine DCs. Using ovalbumin (OVA) as the model antigen, fast-relaxing DCs elicited a CD8+-biased response in vitro, with higher antigen-specific CD8+ T cell activation and proliferation. In vivo adoptive cell transfer of mechanically educated DCs demonstrated that the fast-relaxing matrix licensed DCs to induce a potent draining lymph node T cell response with more antigen-specific T cells and higher restimulation potential. We further showed that DCs sensed matrix stress relaxation through PI3K signaling and actin branching, mediated by the concerted signaling of IL-4 and GM-CSF. Together, these findings demonstrate the role of matrix stress relaxation on the functional state of DCs and suggest a novel approach to enhance ex vivo cellular engineering by targeting mechanical signaling.

ABCA4-associated retinopathies (Stargardt disease) are the most common inherited macular dystrophy and a leading cause of early onset central vision loss. Biallelic pathogenic variants in the ABCA4 gene cause impaired clearance of retinoid byproducts, leading to toxic bisretinoid accumulation, retinal pigment epithelium dysfunction, and progressive photoreceptor degeneration. Clinical presentation and disease progression are highly heterogeneous, largely influenced by genotype, age at onset, and environmental modifiers. Current management remains supportive and includes low-vision rehabilitation and counseling. Recent advances in molecular genetics, retinal imaging, and translational science have substantially expanded the therapeutic pipeline for ABCA4 retinopathy. Disease-modifying strategies under active investigation include visual-cycle modulation, deuterated vitamin A analogs, retinol-binding protein antagonists, gene augmentation and editing approaches, antisense oligonucleotides, and cell-based regenerative therapies. Several pharmacologic agents have demonstrated promising structural outcomes in clinical trials, while gene-based and regenerative approaches continue to evolve amid challenges related to gene size, delivery efficiency, and long-term safety. Optogenetic therapy has emerged as a gene-agnostic option for functional vision restoration in advanced disease stages. This review provides an integrated overview of ABCA4 retinopathy, summarizing disease mechanisms, current management strategies, emerging therapies, and the evolving clinical trial landscape. Emphasis is placed on stage-adapted treatment paradigms, appropriate monitoring endpoints, and the potential role of combination therapies. Ongoing innovation and precision-based approaches offer cautious optimism for durable disease modification and functional preservation in this currently untreatable condition. Stargardt disease is the most common inherited condition that damages the center of the retina and causes vision loss, often beginning in childhood or early adulthood. The disease results from changes in a gene called ABCA4, which normally helps to remove waste products created when the eye processes light. When this system fails, harmful substances build up in the retina. These substances, known as lipofuscin, damage light-sensing cells and lead to a gradual loss of central vision. At present, no approved treatment can stop or reverse this process. Researchers have developed several new treatment strategies based on a better understanding of how the disease works. Some medicines aim to slow the formation of toxic byproducts in the retina by modifying vitamin A metabolism. Early clinical trials suggest that certain compounds may slow the growth of retinal damage in patients with milder disease. Other approaches attempt to replace or repair the faulty ABCA4 gene to address the root cause of the disorder. These gene-based therapies have reduced harmful buildup in animal studies and are now being tested in people. For patients with advanced disease, where many light-sensing cells have already been lost, scientists are exploring cell transplantation and optogenetics. Optogenetics is a technique that makes remaining retinal cells sensitive to light, enabling the restoration of some visual function. Future treatment will likely combine several strategies tailored to the stage of disease, with the goal of preserving vision for as long as possible and restoring function when feasible.

Mechanosensing and mechanotransduction are essential for all living cells. In mammals, Piezo1 and Piezo2 are two mechanically activated cation channels that serve as mechanosensors for a variety of physiological and pathological processes, ranging from touch sensing to sickle cell disease. These two channels are well evolutionarily conserved, and orthologous genes can be traced back to the origin of vertebrates, which underwent whole-genome duplications (WGDs). The number of paralogous genes originating from the vertebrate WGD varies across gene families. Thus, whether there are more PIEZO paralogous genes in vertebrates remains understudied. Here, we identified piezo3 , a new paralog of the piezo gene family, and analyzed its evolutionary history using phylogenetic and synteny analyses. The piezo3 gene is present in most vertebrate lineages but absent in birds and most mammals, likely due to nonfunctionalization after WGDs. In addition, we demonstrated that this channel could mediate calcium flux in response to mechanical stimuli in HEK293T cells, suggesting that Piezo3 exhibits PIEZO1/2-like activation and conduction channel functions. Our CRISPR mutation analysis revealed that the zebrafish piezo3 gene is not developmentally essential, possibly because its expression overlaps with other PIEZO channels. Mutant zebrafish showed elevated sensitivity to mechanical force and increased locomotor activity under (photopic) light illumination. Our results suggest that this new mechanical-sensing Piezo channel is widespread in vertebrates and may be critical for vertebrate adaptation by modulating mechanical sensing and light responses during evolution. All living cells must sense mechanical forces, whether endogenous or exogenous, and respond to them by transforming these forces into biological signals, which is essential to a wide range of cellular processes, including cell division, growth, and differentiation. PIEZO channels are well-characterized, critical, versatile mechanotransducers for touch and pain physiology and for human diseases. Currently, PIEZO1 and PIEZO2 are the only two known PIEZO channels in most vertebrates. In zebrafish, there are two Piezo2 channels (Piezo2a and Piezo2b) due to extra genome duplication in the ray-finned fishes. Here, we report Piezo3 channel, a long-missing paralog of Piezo1 and Piezo2, in most vertebrates. This channel is present in the majority of vertebrate lineages, except for most birds and mammals. The zebrafish piezo3 gene is expressed during early embryogenesis, and mutation of this gene leads to zebrafish larvae responding to tapping mechanical force and light with active movement. The widespread distribution of this Piezo3 channel across most vertebrate species, but its absence in birds and most mammals, suggests it may play important roles in vertebrate physiology and evolution.

Cell-free protein synthesis (CFPS) has emerged as a promising platform for point-of-care (POC) biosensing due to its programmability, rapid response, and ability to operate without living cells. Integrating CFPS into solid-state materials is essential for enabling long-term storage, portability, and spatial multiplexing required for practical POC applications. While previous efforts have demonstrated CFPS integration onto two-dimensional substrates such as paper, embedding CFPS machinery within a three-dimensional matrix that preserves its activity remains a significant challenge. Here, we propose a solid-state CFPS system comprised of a parylene-based scaffold loaded with CFPS machinery, i.e., CFPS in porous parylene (CinPP). The CinPP is fabricated through ice-templated chemical vapor deposition (CVD). We further demonstrate protein synthesis that is readily activated upon rehydration. The CinPP platform supports protein expression after prolonged storage and enables spatially localized and programmable expression of distinct fluorescent proteins. Furthermore, selective reconstitution of CFPS machinery with target-responsive genetic circuits demonstrates its potential as a modular sensing platform. This approach provides a versatile solid-state CFPS material that can be extended to programmable biosensors, portable diagnostic devices, and on-demand protein production systems.

Bacteria encode hundreds of immune pathways that protect host cells against infection by bacteriophages. While immune pathways possess exquisite mechanisms for self-regulation to avoid aberrant activation, many are also tightly regulated at the level of transcription. Many immune operons are regulated by CapP+CapH, a two-protein transcriptional regulator system that triggers immune operon expression in response to DNA damage, by sensing the presence of single-stranded DNA byproducts of DNA damage repair. Here we define how the CapP peptidase is activated by single-stranded DNA. DNA binding in a conserved inter-domain groove in CapP triggers rearrangement of the autoregulatory "cysteine switch loop", opening the active site and allowing binding and cleavage of CapH, which in turn leads to transcriptional activation of an associated immune operon. Our data define a conserved molecular mechanism for sensing bacteriophage infection via DNA damage, and for triggering increased expression of immune operons in response.

Quorum sensing (QS) enables Pseudomonas aeruginosa to coordinate virulence and biofilm formation through cell density-dependent signaling. In clinical isolates from patients with cystic fibrosis (pwCF), mutations in canonical QS systems such as lasR and rhlI often lead to altered signaling hierarchies that complicate our understanding of QS regulation during chronic infection. Here, we dissect the relative contributions of the autoinducer N -butyryl-L-homoserine lactone (C 4 HSL) and the protein binding partner PqsE to RhlR-dependent transcription in CF clinical isolates. Using site-directed mutagenesis to generate RhlR and PqsE variants incapable of responding to C 4 HSL (RhlR A44M) or dimerizing to interact with RhlR (PqsE NI ), we show that both inputs are essential for the full expression of QS-regulated virulence factors, including pyocyanin and rhamnolipids. Transcriptomic analyses revealed that C 4 HSL and PqsE co-regulate a conserved set of 28 RhlR-dependent genes, encompassing canonical virulence loci as well as uncharacterized genes that are likely important for adaptation to the CF airway environment. These findings establish that clinical isolates maintain functional QS circuitry reliant on dual activation of RhlR by both C 4 HSL and PqsE, revealing a conserved regulatory module that underpins pathogenic behavior across genetically diverse isolates. Understanding quorum-sensing regulation in clinical isolates of Pseudomonas aeruginosa is essential to determine how the pathogen persists and adapts within the cystic fibrosis lung. While most studies have focused on laboratory strains, chronic isolates exhibit distinct genetic and regulatory adaptations that complicate our ability to generalize quorum sensing function. Our work defines the coordinated roles of C 4 HSL and PqsE in activating RhlR-dependent gene expression and virulence factor production in isolates from patients with cystic fibrosis. We identify a conserved core of quorum-sensing-regulated genes that remain dependent on both signals despite extensive genomic divergence. These findings highlight that, even within the evolutionary landscape of chronic infection, quorum-sensing signaling through RhlR remains a central and conserved determinant of virulence. By resolving the dual contributions of acyl-homoserine lactone and PqsE-mediated activation, this work provides a mechanistic foundation for future efforts to therapeutically target quorum-sensing pathways in clinical P. aeruginosa infections.

Pressure injuries (or pressure ulcers) are localised damage to skin or tissue (or both) occurring over bony prominences, resulting from prolonged pressure or shear forces (or both). Adults receiving care in any healthcare setting can develop pressure injuries. Immobility, malnutrition, and reduced sensation are some known risk factors. Regular repositioning is a theoretically sound prevention strategy that is part of standard patient care. This is the second update of a review published in 2014 and updated in 2020. To evaluate the benefits and harms, and cost-effectiveness, of repositioning regimens (i.e. repositioning frequencies, position, micromovement) for pressure injury prevention in adults in acute, long-term, or aged healthcare settings, compared to standard care or another repositioning regimen. To identify studies for inclusion in the review, we searched the Cochrane Central Register of Controlled Trials, Ovid MEDLINE, Embase, EBSCO CINAHL Plus, and trial registries on 7 May 2025. We also scanned the reference lists of included studies, reviews, meta-analyses, and health technology reports. We included randomised controlled trials that assessed the effects of any repositioning regimen and measured pressure injury incidence in adults (at least 18 years of age) without an existing pressure injury, in any acute, long-term, or aged healthcare setting. The primary outcome was the cumulative incidence of pressure injuries (any category/stage). Secondary outcomes were health-related quality of life, procedural pain, patient satisfaction, pressure injury prevention and treatment costs, and incremental costs per pressure injury avoided. We assessed the risk of bias in the evidence using the Cochrane RoB 2 tool. We evaluated the certainty of the evidence using GRADE methodology and GRADEpro software. Seven review authors were involved in independently undertaking study selection, data extraction, and RoB and GRADE assessment. All outcomes were binary and reported as risk ratios (RR) with 95% confidence intervals (CI). We pooled data using the fixed-effect or random-effects model, depending on clinical and methodology heterogeneity. We found three new trials. This 2026 update of the review therefore includes 11 trials, which were conducted in acute and aged healthcare settings, and involved 4462 participants aged 18 to 90 years. No new economic substudies were identified, so our cost analysis is based on the two economic evaluations that were included in the previous version of the review. Primary outcome: incidence of new pressure injury (any category/stage) Repositioning frequencies Five trials evaluated different repositioning frequencies in intensive care unit (ICU) and nursing home settings. We pooled the results of four trials that compared 2- versus 4-hourly repositioning (RR 1.05, 95% CI 0.79 to 1.39; 4 trials, 1104 participants), but we judged the certainty of the evidence as very low. There were three other comparisons of repositioning frequencies: 2-hourly versus 3-hourly (RR 1.10, 95% CI 0.30 to 4.08; 3 trials, 795 participants); 3-hourly versus 4-hourly (RR 0.99, 95% CI 0.22 to 4.43; 3 trials, 776 participants); and 4-hourly versus 6-hourly (RR 0.73, 95% CI 0.53 to 1.02; 1 trial, 129 participants). We judged the certainty of the evidence for these results as very low. Therefore, for comparisons of different repositioning frequencies, the evidence is very uncertain. One trial evaluated real-time wearable patient sensor data with visual reminders for 2-hourly repositioning compared to standard care (real-time patient sensor data without visual reminders and with nurse-initiated repositioning) in 1226 ICU patients. The study reported a significant reduction in pressure injuries with the visual warnings from the sensors (RR 0.28, 95% CI 0.10 to 0.75). We judged the certainty of this evidence as moderate. Position Four trials evaluated patient position. Two of the trials compared 30&#xb0; tilt (and 3-hourly repositioning overnight) versus 90&#xb0; tilt (and 6-hourly repositioning overnight) in acute and nursing home patients. We pooled their data and found an RR of 0.62 (95% CI 0.10 to 3.97; 2 trials, 252 participants), but we judged the certainty of this evidence as very low. One trial (120 participants) compared 30&#xb0; and 45&#xb0; tilts with 'usual care' in three ICUs and reported no pressure injuries in either trial arm, but we judged the certainty of this evidence as very low. One trial (116 participants) compared prone versus supine positioning in ICU patients, and found there may be higher pressure injury incidence in the prone group (RR 4.55, 95% CI 2.31 to 8.98). We judged the certainty of this evidence as low. Micromovement We pooled two trials comparing micromovement with standard care (silicone foam dressing) in operating rooms. The results suggested a reduction in pressure injuries with micromovement (RR 0.28, 95% CI 0.11 to 0.67; 2 trials, 477 participants), but the number of events was low. We judged the certainty of the evidence as low. Secondary outcomes No trials reported health-related quality of life, procedural pain, or patient satisfaction. Cost analysis Two trials, both conducted in nursing homes, included parallel economic evaluations. One compared costs of 2-hourly repositioning (321 participants) versus 3-hourly (326 participants) and 4-hourly (295 participants) schedules, with costs being $11.05 and $16.74 (Canadian dollars) less per resident per day for the 3- and 4-hourly regimens, respectively. The other compared 3-hourly repositioning using a 30&#xb0; tilt versus standard care (6-hourly with a 90&#xb0; lateral rotation) in 213 participants. It found that the intervention was cost-effective (EUR 206.60 versus 253.10, incremental difference EUR 46.50, 95% CI 1.25 to 74.60), with a projected annual saving of EUR 512,800 (equating to 21,462 nursing-care hours). Repositioning is a frequently used strategy for pressure injury prevention in adult patients in acute, long-term, and aged healthcare settings. This updated review includes three new trials, but the findings and conclusions align with our earlier reviews. Most of the evidence is of low or very low certainty. There is a lack of robust evaluation of repositioning regimens for pressure injury prevention, and studies are small, resulting in uncertainty about the review findings. There are limited economic evaluation data, making it difficult to reach reliable conclusions about the relative costs of different repositioning regimens. None REGISTRATION: Protocol (2012) DOI: 10.1002/14651858.CD009958.

The assessment of cystic fibrosis transmembrane conductance regulator (CFTR) activity is essential to both diagnose and evaluate the efficacy of treatments in cystic fibrosis (CF). In particular, the prompt evaluation of genotype-specific responses to CFTR modulators might lead to more precise therapeutic approaches. In this study, a flexible electrochemical sensor modified with silver nanoparticles was developed and applied for the electrochemical quantification of chloride ions in CF epithelial cell models. The sensing platform exhibited a linear analytical response toward chloride in both aqueous solutions and chloride-free buffer, with limits of detection in the submillimolar range, enabling the discrimination of chloride concentrations under various conditions. Chloride ions were detected in apical surface liquids obtained from epithelial cultures carrying different CFTR pathogenic variants: the effect of the elexacaftor/tezacaftor/ivacaftor (ETI) treatment, as a CFTR modulator, was differentiated from untreated samples. Chloride concentrations were determined by differential pulse voltammetry using the standard addition method, and results were further normalized to express chloride secretion considering the final apical fluid volume. ETI treatment induced genotype-dependent increases in chloride secretion, with the largest functional recovery observed in responsive genotypes such as F508del/F508del and L1077P/L1077P. A strong correlation was found between chloride levels and normalized secretion rates, confirming how direct electrochemical measurements reliably reflect CFTR functional changes. Overall, this work demonstrates that portable sensors provide a rapid, cost-effective, and scalable approach for functional CFTR evaluation, supporting their potential application in the personalized assessment of CFTR modulator efficacy, namely theratyping.

Real-time, in situ monitoring of neurochemical dynamics in intact neural circuits is critical for elucidating brain function. Recent innovations in micro- and nanoelectrode engineering have markedly advanced our ability to detect neurotransmitter and neuromodulator release with high spatiotemporal resolution, while the application of machine learning (ML) has facilitated the development of next-generation electrodes and enhanced signal processing capabilities. Here, we outline a vision for the potential directions for electrode interface design and the deepening integration of ML in in situ neurochemical sensing, illustrating how breakthroughs over the past decade have illuminated these opportunities.

Two naphthalene diimide (NDI)-based coordination polymers (CPs), namely {[Cd(BENDI)]&#xb7;DMF&#xb7;H2O}n (MDJNU-25) and {[Cd(BENDI)]&#xb7;DMA&#xb7;H2O}n (MDJNU-26), were successfully synthesized via a solvothermal method using Cd(NO3)2&#xb7;4H2O and N,N'-bis(4-ethylphenyl)-1,4,5,8-naphthalene diimide (H2BENDI) in DMF and DMA, respectively. Both CPs exhibit reversible photochromic, electrochromic, and thermochromic properties. Structural analysis reveals that the variation in solvent modulates the crystal packing, resulting in different donor-acceptor (D-A) distances between MDJNU-25 and MDJNU-26. Notably, MDJNU-26 possesses a shorter D-A distance and a faster photoresponse rate than MDJNU-25. Furthermore, both CPs exhibit obvious color changes and high sensitivity to ammonia vapor and organic amines. Fluorescence sensing reveals that elevated antibiotic concentrations enhance quenching, with tetracycline hydrochloride giving the strongest response. The quenching mechanism is attributed to the synergistic effects of the internal filter effect (IFE), fluorescence resonance energy transfer (FRET), and photoinduced electron transfer (PET). TDDFT calculations were used to explore the photochromic and antibiotic-sensing mechanisms. These CPs perform excellently in message encryption and QR code anticounterfeiting, making them promising candidates for multistimuli-responsive systems.