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This study aimed to examine the relationship between foot care behaviours, self-efficacy and diabetes self-care activities among individuals with and without diabetic foot wounds and to identify associated sociodemographic and disease-related factors. A cross-sectional study was conducted with 120 patients presenting to the internal medicine, endocrinology, and diabetic foot outpatient clinics and wards of three different hospitals. Data were collected using a demographic and clinical characteristics form, the Foot Care Behaviour Scale, Diabetic Foot Care Self-Efficacy Scale, and Diabetes Self-Care Scale. Data were analysed using IBM SPSS version 22, with Mann-Whitney U, Kruskal-Wallis H, independent samples t-test, ANOVA and correlation analysis applied as appropriate. Patients with and without diabetic foot wounds did not differ significantly in foot care behaviours or diabetes self-care scores (p&#x2009;>&#x2009;0.05). However, diabetic foot care self-efficacy scores were significantly higher among patients without diabetic foot wounds (p&#x2009;<&#x2009;0.05). In patients with diabetic foot wounds, prior foot care education was associated with significantly higher diabetic foot care self-efficacy and diabetes self-care scores (p&#x2009;<&#x2009;0.05). Older age was negatively correlated with scale scores in both groups, whereas higher education level and certain preventive practices (e.g., foot self-examination, checking footwear) were significantly associated with better scores. Strong positive correlations were identified among foot care behaviours, diabetic foot care self-efficacy, and diabetes self-care across all participants (p&#x2009;<&#x2009;0.05). The strong positive associations among foot care behaviours, diabetic foot care self-efficacy, and diabetes self-care underscore the critical role of patient empowerment in disease management. The higher self-efficacy scores in patients without diabetic foot and those who were previously educated on their prevention demonstrate the importance of early, targeted nursing interventions. Implementing structured foot care education prior to the onset of complications may strengthen patient self-efficacy, improve self-care adherence and ultimately prevent the development of diabetic foot wounds.

To evaluate the effectiveness and safety of an endocrinologist-led glucose management (ELGM) model integrating real-time continuous glucose monitoring (RT-CGM) and continuous insulin infusion therapy, compared with conventional glucose management in critically ill patients admitted to the emergency intensive care unit (EICU). In this single-center, retrospective before-after study, adult EICU patients with stays &#x2265;24 hours were included. Patients admitted in 2023 received conventional glucose management (control), whereas those admitted in 2024 were managed using the ELGM model. Endocrinologists served as primary decision-makers, supported by RT-CGM, point-of-care testing, and continuous insulin infusion. Primary outcomes included mean glucose, glycemic variability, proportion of target-range glucose (3.9 - 10.0 mmol/L), and hypo-/hyperglycemia incidence. Secondary outcomes included nosocomial infection, hyperosmolar hyperglycemic state (HHS), length of stay, ventilation duration, and hospitalization costs. A total of 1138 patients were analyzed (ELGM 625; Control 513). Compared with conventional management, the ELGM model was associated with lower mean glucose (9.9 vs. 11.1 mmol/L; P< 0.001) and reduced variability (SD 4.2 vs. 4.9 mmol/L; P< 0.001). Target-range readings were higher (61.11% vs. 51.66%; P< 0.001), and severe hyperglycemia was less frequent (7.45% vs. 13.28%; P< 0.001). Severe hypoglycemia did not differ. Nosocomial infection (15.02% vs. 27.68%) and HHS (1.28% vs. 5.65%) were lower (both P< 0.001). Length of stay and costs were similar, while ventilation duration was slightly longer. An endocrinologist-led glucose management strategy incorporating RT-CGM was associated with improved glycemic metrics and lower rates of severe hyperglycemia and infection, supporting its feasibility in critically ill patients.

Mobile health applications (MHAs) represent a promising low-threshold tool to support obesity treatment. While commercially available MHAs may be most accessible to potential users, concerns exist regarding their quality, data protection, and evidence base. Therefore, this study aimed to systematically identify and evaluate these aspects. A systematic search was conducted in the Apple App Store and Google Play Store, identifying 1220 apps. After a two-stage screening process, n&#x2009;=&#x2009;21 MHAs met the inclusion criteria and were evaluated independently by two raters using the German version of the Mobile App Rating Scale (MARS-G) with the five subscales Engagement, Functionality, Esthetics, Information, and Therapeutic Gain. Additionally, data on general characteristics (including information on the age group targeted and data protection and safety measures), inclusion of established treatment components, and evidence base, were collected. None of the included MHAs explicitly targeted children or adolescents. Concerning privacy and safety, notable deficiencies were identified, particularly with regard to the absence of active confirmation of privacy policy and/or terms of service and a lack of integrated emergency features. Included MHAs demonstrated moderate overall quality (M&#x2009;=&#x2009;3.31, SD&#x2009;=&#x2009;0.50). The lowest ratings were observed on the subscales Information (M&#x2009;=&#x2009;2.74, SD&#x2009;=&#x2009;0.65) and Therapeutic Gain (M&#x2009;=&#x2009;2.39, SD&#x2009;=&#x2009;0.70). Inclusion of all components of evidence-based obesity treatment guidelines was found in only n&#x2009;=&#x2009;5 MHAs (23.8%). Published evidence for effectiveness was identified for only n&#x2009;=&#x2009;2 MHAs (9.5%). The findings indicate a moderate quality level of commercially available MHAs for obesity treatment, with significant deficits in data protection and safety, content, therapeutic value, inclusion of established treatment components, and scientific evidence. To support safe and effective care for those affected by obesity, there is a need for further research and joint efforts (e.g., in terms of translation into routine practice).

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To investigate the potential of sodium-glucose cotransporter 2 inhibitors (SGLT2i) as a less invasive treatment option for mild diabetic macular edema (DMO) via post hoc subgroup analysis. Previous findings were derived exclusively from observational studies, and no interventional trials based on protocol-defined criteria had been conducted. Based on the COMET trial data, this post hoc analysis targeted mild DME cases, defined by baseline central retinal thickness (CRT) &#x2264;375&#x2009;&#x3bc;m and best-corrected visual acuity (BCVA) &#x2264;0.155 (logMAR). Patients were randomized to SGLT2i (luseogliflozin) or sulfonylurea (SU, glimepiride) groups. Mild subgroups were compared with the corresponding non-mild cases. The primary outcome was the 48-week frequency of intravitreal ranibizumab injections (IVRs). In the CRT &#x2264;375&#x2009;&#x3bc;m subgroup, IVR frequency was significantly lower with SGLT2i vs SU (mean 0.5&#x2009;&#xb1;&#x2009;1.0 vs 4.3&#x2009;&#xb1;&#x2009;0.8; P&#x2009;=&#x2009;0.005, adjusted ancova. Cohen's d of 2.1). The cumulative mean number of IVRs was significantly lower in the SGLT2i group than in the SU group (P&#x2009;=&#x2009;0.004, hazard ratio 0.29, 95% confidence interval 0.12-0.67). In the BCVA &#x2264;&#x2009;0.155 subgroup, whose mean CRT exceeded 400&#x2009;&#x3bc;m, no significant difference in IVR frequency was observed between the SGLT2i-treated and SU-treated patients. In addition, no intergroup differences were found in patients outside the mild subgroups. In this exploratory analysis, SGLT2 inhibition was associated with fewer intravitreal injections in patients meeting the CRT-based mild criteria. These findings are hypothesis-generating and warrant confirmation in future prospective studies.

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The human vascular network is a highly dynamic, complex and organ-specific microenvironment essential for organ homeostasis. Traditional 2D cell cultures fail to capture its complex intercellular interactions, tissue-specific architectures, and mechanobiological cues. Blood vessel organoids (BVOs) generated from human induced pluripotent stem cells (hiPSCs) replicate the structure and function of blood vessels. Because hiPSCs preserve the donor's telomere length and epigenetic memory, BVOs may preserve the genesis memory, opening up a completely new avenue for the study of vascular disorders. In this review, we systematically outline the methods for in vitro blood vessel generation and explore how vascularizing parenchymal organoids actively drives tissue maturation while overcoming hypoxic limitations. We assess the vital transition from biochemical induction to biomechanical integration, highlighting how microfluidic organ-on-a-chip (OoC) platforms resolve the lineage-specific media dilemma and impose the physiological shear stress necessary for definitive vascular maturation. Furthermore, we comprehensively summarize the applications of BVOs as personalized preclinical avatars across diverse pathologies, including diabetic vasculopathy, cerebrovascular and cardiovascular diseases, tumor immune evasion, hereditary anomalies, and infectious vasculotropism. Finally, we address critical current bioengineering constraints-notably incomplete vessel maturation, the absence of functional lymphatic systems, and the lack of immunocompetent microenvironments-providing strategic future perspectives to accelerate the translation of BVOs in precision and regenerative medicine.

The role of extracellular acidity in regulating parathyroid hormone (PTH) secretion in cultured mouse parathyroid glands (PTGs) has not studied to date, largely due to the technical difficulty of isolating mouse PTGs. We hypothesized that acidic extracellular pH directly stimulates PTH secretion through activation of a proton-sensing receptor, specifically ovarian cancer G protein-coupled receptor 1 (OGR1, also known as GPR68). To test this, we developed a method to reliably identify and isolate PTGs from male mice by administering 5-aminolevulinic acid (5-ALA), which induced selective fluorescence in these glands. Using this model, we demonstrate that acidic extracellular pH significantly stimulates PTH secretion in cultured mouse PTGs. Mechanistically, we identify OGR1 as the primary proton sensor mediating this response, as PTGs from OGR1 knockout mice failed to increase PTH secretion under acidic conditions, with no evidence of compensatory upregulation of other proton-sensing receptors. In addition, we found that low extracellular Ca2+ not only stimulates PTH secretion but also promotes extracellular acidification. Notably, low Ca2+ and acidic pH act synergistically to enhance PTH secretion in wild-type PTGs, an effect markedly attenuated in OGR1-deficient glands. Together, these findings establish a direct, OGR1-dependent mechanism by which extracellular acidity regulates PTH secretion and reveal an interaction between calcium and pH signaling in this process. This work provides a robust ex vivo model for studying PTG physiology and offers new insight into how metabolic acidosis may contribute to secondary hyperparathyroidism in chronic kidney disease, highlighting OGR1 signaling as a potential therapeutic target.

Hypothalamic arginine vasopressin (AVP) and oxytocin (OXT) magnocellular neurons (MCNs), share a developmental lineage. The transcription factors driving specification are yet unknown. Using gene regulatory network analysis on published single-cell RNA-sequencing data of the developing mouse hypothalamus, we identified RORA, EBF3, FOXP1, FOXP2, and BCL11B as candidate transcription factors for differential MCN specification. We modeled developmental gene expression dynamics using computational cell fate mapping, revealing enrichment of EBF3 and BCL11B in the Avp lineage, and FOXP1 and FOXP2 in the Oxt lineage. In silico analysis of Avp and Oxt promoters predicted a binding site for FOXP1 and FOXP2, and an in vitro reporter assay identified regulation on both Avp and Oxt genomic promoters. Finally, heterozygous FOXP1 knockout mice exhibited a significant reduction in AVP and OXT neuron abundance, with OXT neurons disproportionally affected. We conclude that FOXP1 participates in MCN development, while being differentially active in OXT MCNs relative to AVP MCNs.

Heart failure (HF) is increasingly driven by cardiometabolic risk factors such as obesity and insulin resistance. The estimated glucose disposal rate (eGDR) is a validated surrogate marker of insulin resistance. Reduced eGDR, reflecting higher insulin resistance, has been linked to cardiovascular disease, but its associations with myocardial fibrosis and HF remain unclear. The study included 6025 participants in MESA (Multi-Ethnic Study of Atherosclerosis) free of HF at exam 2 (2002-2004). eGDR was calculated using body mass index, hypertension, and hemoglobin A1c. Cardiac magnetic resonance imaging (2010-2012) assessed left ventricular ejection fraction and myocardial fibrosis by late gadolinium enhancement. Associations of baseline eGDR with incident HF were evaluated using Cox models, stratified by diabetes. Over a mean follow-up of 14&#xb1;5&#x2009;years, 404 participants developed HF. eGDR was inversely associated with incident HF (adjusted hazard ratio [HR] per unit decrease, 1.28 [95% CI, 1.22-1.35]), a relationship that persisted regardless of diabetes status and was more pronounced for HF with preserved ejection fraction (n=200; adjusted HR per unit decrease, 1.36 [95% CI, 1.27-1.45]) than HF with reduced ejection fraction (n=168; HR, 1.19 [95% CI, 1.11-1.27]). Lower eGDR was also associated with higher left ventricular ejection fraction (n=2899; &#x3b2;=0.16, [95% CI, 0.03-0.28]) and higher odds of myocardial fibrosis (n=1780; adjusted odds ratio, 1.27 [95% CI, 1.16-1.41]). Lower eGDR is independently associated with subclinical myocardial damage and incident HF, highlighting insulin resistance as a key driver of adverse remodeling and a potential marker for early HF risk stratification and prevention.

IntroductionRefractory cardiac arrest carries a poor prognosis. Extracorporeal cardiopulmonary resuscitation (ECPR) can be lifesaving but is associated with high morbidity and mortality. We report a likely underdiagnosed complication - non-occlusive mesenteric ischemia (NOMI) - following ECPR, emphasizing the diagnostic challenges and the role of early endoscopic evaluation and an interdisciplinary assessment of these patients.Case PresentationA 48-year-old man presented with ST-elevation myocardial infarction and developed refractory cardiac arrest due to ventricular fibrillation. ECPR was initiated, and extracorporeal membrane oxygenation (ECMO) flow was achieved after 77 min of cardiopulmonary resuscitation. Early after arrest, the patient passed bloody stool, raising suspicion of mesenteric ischemia. Computed tomography was inconclusive, but colonoscopy revealed ischemic bowel injury. Given the fatal potential of untreated NOMI, prompt colectomy was performed. The patient stabilized postoperatively, recovered progressively, and was discharged from the intensive care unit in good condition after 14 days.ConclusionNOMI should be considered in ECPR patients presenting with gastrointestinal bleeding, even when cross-sectional imaging findings are inconclusive. Early colonoscopy enables timely diagnosis and surgical intervention, potentially improving survival in this high-risk setting.

Intestinal obstruction is a common complication caused by colorectal cancer, and the implantation of stents has become an indispensable palliative treatment strategy for non-surgical eligible patients. However, the lack of sustained anti-tumor efficacy and wear caused by configuration or deformation discrepancies has led to the recurrence of stenosis, posing a significant challenge in clinical treatment. Here, we reported an intestine-specific, application-driven 4D-printed sandwich-structured metamaterial intestinal stent platform, achieving the triple goals of sustained anti-tumor effects, customized configuration and performance, and rapid relief of intestinal obstruction. Specifically, the platform comprised an outer Janus layer designed for synergistic photothermal-and-drug anti-tumor effects, an intermediate layer of biomimetic gradient metamaterials for structural support and coordinated deformation, and a hydrophobic inner layer to mitigate the risk of restenosis. Overall, this study presented a multifunctional intestinal stent built upon a scalable design paradigm, offering an innovative and clinically translatable therapeutic strategy for personalized colorectal cancer management.

Primary aldosteronism (PA) can be managed either by unilateral adrenalectomy (ADX) or pharmacologically with mineralocorticoid receptor antagonists (MRA). Several recent meta-analyses have examined how these treatment modalities affect cardiovascular outcomes in patients with PA. However, the impact of treatment on quality of life (QoL) remains largely unexplored. To synthesize data from previous studies that have investigated QoL in either medically or surgically treated patients with PA. A literature search was conducted in May 2025 in PubMed, Embase and Web of Science. Studies containing data on QoL before and after ADX or MRA were selected. Fifteen studies evaluated QoL after treatment for PA. Most comparative studies reported greater and faster QoL improvement after ADX than with MRA. QoL consistently improved after ADX, whereas results with MRA were variable and less consistent. Patients treated with MRA were older than patients treated with ADX and frequently received low MRA doses. Five studies (259 ADX-treated and 88 MRA-treated patients) were included in a meta-analysis. Baseline QoL did not differ between treatment groups. At 6 months, QoL improved in both groups, with no statistically significant difference between ADX and MRA. Treatment of PA is associated with improved QoL following both ADX and MRA therapy. Although several studies suggest superior outcomes after adrenalectomy, the meta-analysis did not show a significant difference at 6 months of follow-up. The limited number of patients, short follow-up duration, and potential undertreatment with MRA represent important limitations.

This study aimed to investigate the correlations of serum uric acid (SUA) and glycated hemoglobin (HbA1c) levels with mild cognitive impairment (MCI) in patients with comorbid type 2 diabetes mellitus (T2DM) and hypertension, and to further identify potential risk factors associated with MCI. In this retrospective study, 126 older patients with T2DM and hypertension were divided into a normal cognition group (n&#x2009;=&#x2009;74) and an MCI group (n&#x2009;=&#x2009;52) based on Mini-Mental State Examination (MMSE) scores. The correlations of SUA and HbA1c with MMSE scores, their predictive value for MCI, their relationships with clinical variables, and independent risk factors for MCI were evaluated using Spearman correlation, receiver operating characteristic curve, and logistic regression analyses. In the MCI group, SUA and HbA1c levels were significantly negatively correlated with MMSE scores (r&#x2009;=&#x2009;-0.419 and -0.510). For predicting MCI, the area under the ROC curve (AUC) was 0.742 for SUA (sensitivity: 78.85%, specificity: 62.16%, cut-off value: 319.31), 0.781 for HbA1c (sensitivity: 48.08%, specificity: 94.59%, cut-off value: 8.94), and 0.851 for their combination (sensitivity: 73.08%, specificity: 85.14%, cut-off value: 0.42). Elevated SUA and HbA1c levels and older age were independent risk factors for MCI, whereas higher IBIL and HDL-C levels and reading habits were protective factors. SUA and HbA1c levels were elevated in older patients with T2DM and hypertension who developed MCI. These markers were identified as independent risk factors for MCI in patients with T2DM-hypertension, aiding in the prediction of MCI occurrence in these patients.

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Hashimoto's thyroiditis (HT) is a common disease characterized by autoimmune injury of the thyroid. Its pathogenesis entails complex interactions among hereditary predisposition, immune disorders and environmental factors. In recent years, viral infection has attracted much attention as a potential environmental trigger, but the role genes associated with HT remain unclear. In this study, COVID-19-related genes were combined with transcriptome data (GSE29315, GSE138198) of HT patients in the GEO database. Key genes were selected using machine learning (LASSO, SVM, and RF), GO/KEGG enrichment, and GSEA. Its function was confirmed by single-cell sequencing and ssGSEA immunoinfiltration analysis. A total of 16 co-expressed genes of HT and viral infection were identified. KEGG and GO enrichment results showed that these genes were significantly enriched in inflammatory signaling, viral defense and immune cell activation pathways. After screening by machine learning algorithm, four key genes (IFITM3, IFI44L, CCL3, OAS1) were finally identified as the common diagnostic markers of HT and viral infection, and the ROC curve also showed good diagnostic performance. In addition, single cell sequencing further confirmed its high expression in thyroid tissue and immune infiltrating cells. A virus-triggered autoimmune cascade involving IFITM3, IFI44L, CCL3, and OAS1 may precipitate HT. These four genes constitute robust, multi-omics biomarkers for early diagnosis and targeted therapy of HT following viral infection.

Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease (ESRD) worldwide. Blood pressure variability (BPV), especially diastolic BPV (DBPV), is closely linked to renal microcirculation but remains understudied in DKD. This study aimed to evaluate the association of DBPV with renal progression, identify an optimal risk threshold, and explore antihypertensive drug implications. We conducted a retrospective cohort study of 2,143 DKD patients who underwent 24-hour ambulatory BP monitoring (ABPM) between 2018 and 2022, with a median follow-up of 4.8 years. Multiple DBPV parameters including standard deviation (SD), coefficient of variation (CV), average real variability (ARV), and nocturnal dipping were analyzed. Dynamic changes in DBPV were assessed in 1,328 patients with serial ABPM data. After full adjustment, 24-hour DBP ARV was the strongest predictor of renal outcomes. Each 1 mmHg increase was associated with 18% higher odds of rapid estimated glomerular filtration rate (eGFR) decline (OR&#xa0;=&#xa0;1.18, 95%CI:1.13-1.23), 22% higher ESRD risk (HR&#xa0;=&#xa0;1.22, 95%CI:1.15-1.29), and 20% higher composite renal event risk (HR&#xa0;=&#xa0;1.20, 95%CI:1.14-1.26). ROC analysis determined the optimal threshold of 24-hour DBP ARV for ESRD prediction as 10.2 mmHg (sensitivity=76.2%, specificity=61.8%), above which ESRD risk increased 3.1-fold. Patients with increased DBPV over time had a 2.4-fold higher ESRD risk than those with decreased DBPV. Calcium channel blockers (CCBs) were associated with lower DBP ARV than RAAS inhibitors or beta-blockers. Adding 24-hour DBP ARV to traditional risk models significantly improved ESRD prediction (C-statistic: 0.73 to 0.80). The association was stronger in patients with advanced DKD or severely increased albuminuria, and combined high DBP ARV and SBP ARV conferred a 4.5-fold higher ESRD risk. 24-hour DBP ARV (threshold 10.2 mmHg) is an independent predictor of renal progression in DKD. Rising DBPV amplifies renal risk, and CCBs may better reduce DBPV. Incorporating ABPM-derived DBPV into DKD management improves risk stratification and supports personalized interventions.

To develop a deep learning-based multimodal framework for automated segmentation of orbital soft tissues and identify quantitative imaging biomarkers for precise grading of thyroid eye disease (TED). This retrospective multicenter study enrolled 330 TED patients from a primary center for model development and 113 patients from two external centers for validation. From the primary cohort, 182 mild and 138 moderate-to-severe TED were subsequently selected for further analysis. All subjects underwent 3&#x2009;T MRI with water-fat separation and fat-suppressed (FS) T2 mapping sequences. TED-Net, a deep learning model integrating ConvNeXt and Transformer architectures, was developed to segment orbital structures including the extraocular muscles, lacrimal gland, orbital fat, and eyeball. The model automatically extracted both morphological parameters (volume and volume ratio) and functional parameters (water fraction, fat fraction, and FS T2 relaxation time), enabling quantitative comparison between mild and moderate-to-severe TED. Diagnostic performance for evaluating orbital involvement was assessed using receiver operating characteristic analysis and decision curve analysis. TED-Net achieved Dice similarity coefficients&#x2009;>&#x2009;0.80 across all orbital structures. Volumetric measurements showed high consistency among different sequences (intraclass correlation coefficient&#x2009;=&#x2009;0.843). Significant differences in morphological and functional parameters were observed between mild and moderate-to-severe TED (all p&#x2009;<&#x2009;0.05). The combined volumetric-functional model demonstrated superior diagnostic accuracy (area under the curve [AUC]&#x2009;=&#x2009;0.982) over the volumetric model (AUC&#x2009;=&#x2009;0.908). TED-Net enables accurate automated segmentation and multiparametric quantification of orbital soft tissues, providing reliable imaging biomarkers for objective assessment of TED severity. Question MRI-based quantitative metrics are essential for assessing orbital involvement in TED, but effective tools for rapid and accurate parameter extraction are currently lacking. Findings TED-Net achieved precise orbital segmentation and multiparametric quantification; the integration of volumetric and functional parameters yielded an AUC of 0.982 for evaluating orbital involvement. Clinical relevance The proposed TED-Net provides a reliable approach for quantifying orbital soft tissue involvement, and its clinical implementation enables more accurate assessment of TED severity.