Despite substantial investment in health information technology, evidence on whether advanced nursing documentation systems improve patient outcomes remains limited. This study examined whether system sophistication, utilization, user satisfaction, and process alignment predict hospital-acquired pressure injury (HAPI) rates in German hospitals. Secondary analysis of 2023 data from the IT-Report Healthcare linked with German quality registry data (IQTIG) was conducted using post-stratified weighted regression models. System utilization degree averaged 66.0%, user satisfaction 6.69/10, process alignment 7.11/10, and IT sophistication 11.3/30. Neither system utilization (p=0.964), satisfaction (p=0.962), process alignment (p=0.950), nor IT sophistication (p=0.552) showed significant associations with HAPI rates. Hospital size and ownership predicted HAPI outcomes, while reverse analysis revealed that hospitals with low HAPI quality (high ratios) expressed greater desire for advanced functionality (OR=2.08, p=0.031). Findings suggest that technology deployment alone cannot improve pressure injury prevention. Obviously wound care related software is not advanced enough to make a difference as there is a wish better support.

Clinical guidelines (GLs) standardize care but are complex to implement. Most clinical decision support systems (CDSSs) assume continuous use, which does not reflect real-world episodic workflows. We developed and evaluated e-Picard, a CDSS providing GL-based recommendations for episodic, on-demand consultations, enabling prospective decision support informed by retrospective quality assessment. At runtime, e-Picard analyzes offline patient data, computes fuzzy-logic-based compliance, identifies missed actions and generates context-specific recommendations. The system was applied to longitudinal geriatric data managed under pressure ulcers (PU) and diabetes (DM) GLs. Manual technical validation using 3,110 PU and 12,538 DM data instances (43 PU and 82 DM patients) achieved ≥99% correctness and up to 98% completeness. Retrospective simulation on 1,000 patients per domain (57,860 PU and 100,940 DM data instances) demonstrated potential adherence improvements from 68%-69% to 89%-97% for PU and from 14%-15% to 60%-87% for DM, with higher consultation frequencies increasing compliance and reducing care variability. These results demonstrate that episodic CDSSs can deliver accurate, context-aware support even under intermittent use.

Cerebral infarcts in carotid artery disease arise from a complex interplay between plaque vulnerability, extracranial vascular burden, intracranial collateral capacity. Although each of these factors has been studied individually, their combined impact on infarct presence, infarct pattern, and long-term outcomes in real-world carotid endarterectomy (CEA) populations remains insufficiently understood. This study aimed to determine how carotid plaque morphology, bilateral carotid stenosis severity, circle of Willis (CW) anatomy jointly influence ipsilateral brain infarcts and overall mortality. We retrospectively analyzed 1,304 CEA patients using standardized CT and CT angiography to assess plaque features, maximal plaque thickness, carotid stenosis burden (carotid score), detailed CW configuration. Ipsilateral cerebral infarcts were classified as territorial or watershed. Logistic regression was used to determine predictors of infarcts and infarct pattern, Cox proportional-hazards models assessed long-term mortality. Reproducibility of plaque composition and thickness assessment was evaluated in 100 patients using Cohen's kappa and intraclass correlation coefficient. Ipsilateral infarcts were present in 36.7%. Independent predictors included symptomatic status, greater plaque thickness, exulcerated plaques, more advanced bilateral carotid disease (lower carotid score), severely compromised CW. Lower carotid scores predicted watershed infarcts, supporting a hemodynamic mechanism; exulcerated plaques predicted territorial infarcts, consistent with distal embolization. Long-term mortality was independently associated with age, diabetes mellitus, chronic obstructive pulmonary disease, severe chronic kidney disease, the presence of ipsilateral infarcts, type-1 CW anatomy, and calcified plaques. In conclusion, plaque vulnerability, extracranial vascular burden, CW integrity provide complementary, clinically meaningful information on the development and pattern of brain infarcts and on long-term survival after CEA. These findings underscore the importance of comprehensive cerebrovascular imaging for risk stratification and individualized management of carotid artery disease.

Genetic colocalisation analyses are frequently conducted to determine if causal signals at a genetic locus are shared between two phenotypes. However, colocalisation is rarely undertaken at the HLA locus, due to its complex linkage disequilibrium (LD) and high polymorphism density. This lack of genetic causal inference method limits our ability to translate HLA associations into therapeutic targets. Here we present a method that uses HLA alleles, instead of nucleotide variants, to perform genetic colocalisation of two traits at HLA genes. The method, which we call HLA-colocalisation, works by controlling for LD using a Bayesian variable selection algorithm (here implemented with SuSiE), then performing Bayesian regression on the resulting posterior inclusion probabilities. We first show through simulation that the method correctly identifies truly colocalising genes. We then test the method in two positive control scenarios, showing colocalisation between hepatitis B and liver disease at HLA-DPB1, and between Epstein-Barr virus and multiple sclerosis at HLA-DRB1 and HLA-DQB1. Finally, we perform a large colocalisation scan between multiple viruses and auto-immune diseases, demonstrating that the method is well calibrated and uncovering multiple biologically plausible novel causal associations, such as cytomegalovirus and ulcerative colitis. To our knowledge, HLA-colocalisation is the first accurate genetic colocalisation method for the HLA locus (github: https://github.com/DrGBL/hlacoloc).

PANoptosis is a novel programmed inflammatory cell death pathway. It integrates pyroptosis, apoptosis, and necroptosis components via a unified molecular platform termed PANoptosome. Unlike single classical cell death pathway, PANoptosis is tightly regulated by key regulators such as ZBP1, RIPK3, caspase-8, and ASC, resulting in a highly inflammatory and immunogenic form of cell death. While its pathological relevance has been widely investigated in cancer, microbial infections, and systemic inflammatory syndromes, its role in intestinal diseases has not been comprehensively explored. In this review, we summarize emerging evidence highlighting its key role in intestinal diseases, including Crohn's disease, ulcerative colitis, colorectal cancer, intestinal ischemia/reperfusion injury, necrotizing enterocolitis, celiac disease, and immune checkpoint inhibitors-induced colitis. We further summarize recent advances in PANoptosis mechanisms and immunological regulation in intestinal diseases, highlight its intricate interplay with gut microbiota, and discuss the therapeutic potential of targeting PANoptosis to restore intestinal homeostasis and mitigate disease progression.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease affecting the colonic mucosa. Changes in mucin phenotype may be associated with mucosal inflammation in UC. However, the relationship between clinicopathological features and mucus phenotypes in UC remains unclear. Therefore, we aimed to evaluate the association between mucus phenotypes and clinicopathological features in patients with UC using immunohistochemistry, as well as their association with ultra-high magnification endocytoscopy (EC) classification. A total of 51 lower gastrointestinal endocytoscopy procedures were performed for 39 patients with UC between 2018 and 2022. MUC2 expression was positive in all biopsy specimens, whereas MUC1, MUC6, and CD10 expression was negative. MUC5AC was expressed in 51.3% of cases. MUC5AC positivity was associated with duration of disease, classification by clinical course, Mayo score, Mayo endoscopic subscore (MES), Nancy histological index, C-reactive protein levels, erythrocyte sedimentation rate, and EC classification at the patient level. At the specimen level, significant differences were observed in the Nancy histological index, MES, and EC classification. In multivariate analysis, the Nancy histological index showed a significant correlation.MUC5AC is strongly correlated with histopathological severity and may also be associated with clinical and endoscopic severity. The clinical significance of MUC5AC positivity remains a topic for future investigation.

Ulcerative colitis (UC) and periodontitis, both microbial dysbiosis-driven chronic inflammatory disorders, coexist and mutually exacerbate, but the causal mechanisms remain unclear. Using ligature-induced periodontitis plus DSS-colitis mice, we found UC doubles alveolar bone loss, heightens systemic inflammation, oxidative stress, and osteoclastogenesis. 16S rRNA and LC-MS metabolomics showed UC enriches oral pathogens, depletes gut Firmicutes, expands Bacteroides, and correlates with suppressed amino-acid/bile-acid biosynthesis. Fecal microbiota transplantation (FMT) from DSS donors into antibiotic-pretreated periodontitis-prone mice replicated aggravated bone loss, systemic inflammation, gut-barrier leakage, and Th17/Treg imbalance, while healthy-donor FMT protected. GC-MS revealed 35-60% reductions in acetate, propionate, and butyrate; keystone taxa Parabacteroides and Muribaculum inversely correlated with SCFAs and host inflammatory genes. Collectively, UC-driven gut dysbiosis is a transmissible causal factor that simultaneously remodels oral and intestinal biofilms, erodes epithelial barriers, and amplifies osteoclastic bone resorption. SCFAs-producing microbes or supplementation may be potential therapeutics for UC-associated periodontitis patients.

Ulcerative colitis (UC) is closely linked to intestinal barrier dysfunction and gut dysbiosis. Bacterial extracellular vesicles (bEVs) act as key mediators of bacteria-host crosstalk, with great potential in regulating host health. Recent studies have shown that EVs derived from gut commensal bacteria offer therapeutic advantages in treating UC. Herein, we explored the therapeutic effect of Faecalibacterium prausnitzii-derived EVs (PEVs) in DSS-induced colitis mice. Results showed PEVs significantly improved intestinal barrier damage, restored Th17/Treg balance and alleviated gut dysbiosis. Further fecal microbiota transplantation (FMT) confirmed that feces from PEVs-treated mice transferred beneficial effects to recipient colitis mice. Collectively, our findings indicate that commensal gut microbiota-derived nanovesicles have the potential to serve as candidates for UC treatment.

Mounting evidence suggests that psychosocial stressors, such as social isolation and loneliness, contribute to gastrointestinal disorders by disrupting gut-brain interactions. We aim to investigate the associations of social isolation, loneliness, and their related alterations in metabolism and circulating proteins with the risk of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD). 275,157 adults from the UK Biobank were analyzed, including metabolomic data from 68,362 participants and proteomic profiling from 29,339 participants. The exposures included social isolation, loneliness, and their related metabolites and circulating proteins, with incident IBD as the outcome. Cox regression and two-sample Mendelian randomization (TSMR) analysis were utilized to examine the associations. Over a mean follow-up of 13.49 years, this cohort study identified 1565 incident IBD cases, comprising 1063 UC cases and 492 CD cases. Social isolation and loneliness showed significant associations with an elevated risk of IBD (social isolation: hazard ratio [HR]most isolated: 1.31, 95%CI: 1.01-1.70; loneliness: 1.29, 95%CI: 1.04-1.60). Social isolation and loneliness jointly increased the risk of IBD by 85%, with an HR of 1.85 (95% CI: 1.02-3.36). TSMR analyses further indicated that more sports or gym activity reduced IBD and CD risk, more religious activity lowered UC risk, while fewer leisure/social activities increased UC risk. For the metabolomic analysis, eight and five metabolites were identified to be associated with social isolation and loneliness, respectively. Additionally, 22 circulating proteins consistently associated with both loneliness and social isolation were identified, predominantly enriched in cytokine-related pathways. The derived protein scores were positively associated with an increased risk of IBD. This study demonstrates social isolation and loneliness significantly raise IBD risk, with related metabolite and circulating proteins shedding light on underlying biological mechanisms.

Radiation therapy often causes oxidative stress and inflammation in normal tissues due to the generation of excessive radiation-induced reactive oxygen species (ROS). This can subsequently lead to radiation-induced skin injury (RISI), which manifests as tissue damage ranging from dermatitis to ulcers. One approach to addressing these challenges is to develop biocompatible functional materials that can facilitate repair and improve treatment tolerance by neutralizing ROS. In this study, a water-responsive lipid gel (LG) delivery system was constructed using Kangfuxin liquid (KFX, the ethanol extract of Periplaneta americana L.), soybean lecithin (SPC), and glycerol dioleate (GDO), based on KFX's broad-spectrum free radical scavenging ability, anti-inflammatory properties, and prorepair properties. Due to the molecular self-assembly properties of SPC and GDO, the KFX LG system can physically cross-link to form an in situ gel barrier upon contact with water. The barrier exhibits exceptional tissue adhesion, long-term slow-release properties, and good biocompatibility. The versatile KFX LG system has also been found to effectively remove various types of free radicals and reduce levels of proinflammatory factors. In a mouse model of radiation dermatitis, the radioprotective properties of the KFX lipid gel were demonstrated to be effective in alleviating radiation dermatitis. This study explored the radioprotective potential of KFX LG biomaterials in the context of radiation dermatitis, highlighting the application of radioprotectants as a promising RISI treatment strategy.