Post-stroke dysphagia, which affects 40% to 70% of stroke survivors, frequently leads to aspiration pneumonia and diminished quality of life. Despite achieving a 98.8% initial swallowing screening rate, the nasogastric tube removal rate in our unit of 52.7% was below the national benchmark of 57.4%. A quality control circle root cause analysis was conducted, with five critical issues identified. These included a lack of routine in-service education, insufficient interdisciplinary collaboration, inconsistent screening tool versions being used, a deficit in integrated educational resources, and ambiguous re-screening protocols during patient transfers that resulted in a low re-screening rate (60.3%).

This project was implemented to increase the nasogastric tube removal rate in stroke patients from the baseline of 52.7% to a minimum target of 67.8%.

Four key interventions were implemented using quality control circle methodologies. These included: (1) Organizing interdisciplinary workshops to clarify intervention timing and professional roles across disciplines; (2) Integrating a "Three-Stage Swallowing Screening Tool" incorporating pre-procedural oral hygiene protocols and clinical decision-making algorithms; (3) Developing interdisciplinary patient education materials encompassing nursing, traditional Chinese medicine, and speech-language pathology; and (4) Revising standard operating procedures to mandate re-screening during all inter-unit transfers.

Post-intervention, the nasogastric tube removal rate increased from 52.7% to 69.9%, which exceeded the targeted goal. Notably, no re-intubations occurred within the six-month post-discharge follow-up period. In addition, the re-screening rate during inter-unit transfers improved markedly from 60.3% to 97.4%. Ancillary benefits included redirecting approximately 15 minutes of tube maintenance time per nurse daily into high-value individualized patient care,and an estimated savings in annual healthcare costs of NT$24,708 per family.

The process standardization and enhanced interdisciplinary synergy achieved under this project effectively eliminated gaps in care, resulting in substantially improved patient safety and care quality.

Maternal cardiac arrest occurs in 1 of 12,000 to 36,000 pregnancies and presents with unique etiologies and physiologic considerations. Pregnancy alters resuscitation dynamics, making key modifications to advanced cardiac life support protocols such as left uterine displacement, early and effective airway management, and consideration of perimortem cesarean delivery, crucial for successful resuscitation. Extracorporeal life support may be indicated in refractory cases and must account for unique maternal physiology, like increased oxygen consumption and cardiac output. Despite its complexity, maternal cardiac arrest can have favorable outcomes with timely multidisciplinary care, highlighting the importance of preparedness in maternal code response.

Thrombotic pulmonary and venous embolism remains a leading cause of maternal mortality in the United States, prompting expanded venous thromboembolism prophylaxis guidelines from organizations such as the American College of Obstetricians and Gynecologists, Royal College of Obstetricians and Gynaecologists, American College of Chest Physicians, and American Society of Hematology. Increased pharmacologic thromboprophylaxis, particularly with heparins, complicates decisions regarding neuraxial anesthesia due to the risk of spinal epidural hematoma, while general anesthesia carries higher maternal risks. Guidance from the Society for Obstetric Anesthesia and Perinatology and American Society of Regional Anesthesia and Pain Medicine supports individualized risk assessment.

Scorpion envenomation is an important public health problem in many tropical and subtropical regions and may result in rare but life-threatening grade III complications involving multiple organ systems. This systematic review synthesizes published articles from 2000 to 2025 that describe uncommon, severe clinical manifestations following scorpion stings. A total of 72 rare clinical complications were identified, encompassing cardiovascular, neurological, respiratory, renal, hematological, ocular, dermatological, and other systemic manifestations. Cardiovascular complications were the most frequently reported, whereas neurological complications exhibited the greatest clinical diversity. Mesobuthus tamulus and Hemiscorpius lepturus were most commonly associated with severe complications, and children younger than 10 years appeared to be at increased risk of serious neurological involvement. These findings highlight the remarkable clinical heterogeneity of grade III scorpion envenomation and emphasize the importance of early recognition, species-specific clinical awareness, and timely management to reduce severe outcomes in endemic regions.

The long-term health effects of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) remain unclear. Most importantly, it is highly controversial whether GIP agonists vs. antagonists should be developed and what their effects and/or potential side effects would be in the clinic. Further investigation is needed to explore the effects of GIP lowering alone or in combination with GLP-1 enhancing. Tree-structured phenotypic modeling (TreeWAS) and factorial Mendelian randomization (MR) analyses are valuable in this context, even though the highest circulating GLP-1 levels may reflect only a minimum activation i.e. levels achieved with pharmacological intervention with dipeptidyl peptidase 4 (DPP-4) inhibitors and not GLP-1 receptor agonists (GLP-1 RAs) which achieve much higher levels.

TreeWAS was first conducted to map associations of GLP-1 or GIP levels with a broad range of disease outcomes among 385,917 UK Biobank participants. Disease-trajectory analysis was applied to characterize temporal patterns of co-occurrence of multiple comorbidities related to GLP-1 or GIP or both. Subsequently, factorial MR was performed to investigate the joint effects of GLP-1 and GIP on the associated health outcomes. Finally, mediation analysis was employed to explore the underlying mechanisms through which GLP-1 and GIP exert their effects.

TreeWAS analysis revealed associations of elevated genetically predicted GLP-1 levels, even within the normal range, with decreased risk of metabolic diseases (e.g. type 2 diabetes) and polyarthropathies (e.g. gout). While genetically determined low GIP levels were linked to reduced risk of obesity, metabolic diseases (e.g. disorders of lipoprotein metabolism and other lipidaemias), digestive/hepatic and cardiometabolic diseases. Consistently, disease-trajectory analysis identified four major comorbidity clusters among individuals with genetically proxied physiologically lower GLP-1 and higher GIP levels, primarily involving metabolic diseases (e.g. type 2 diabetes), musculoskeletal system diseases (e.g. gout), gastrointestinal and urinary system disorders. Furthermore, the combined exposure to genetically predicted higher GLP-1 and lower GIP levels were associated with complementary and additive reductions in the risk of obesity (HR = 0.93, 95%CI: 0.88-0.99, p = 0.018), CVD (HR = 0.97, 95%CI: 0.94-0.99, p = 0.021), venous thromboembolism (VTE) (HR = 0.91, 95%CI: 0.83-1.00, p = 0.039), and multiplicative effects on composite hepatic events (CHEs) (HR = 0.88, 95%CI: 0.77-0.99, p = 0.040). No side effects on bone metabolism were identified. Finally, mediation analysis revealed that genetically predicted lower physiological GIP levels were associated with lower risk of obesity, CVD, VTE, overall and cardiovascular-specific mortality, with body weight consistent with a potential mediating role in exploratory decomposition analyses.

Our genetic findings are consistent with the hypothesis that GLP-1 levels in the higher physiological range and GIP levels in the lower physiological range, individually and jointly, may be associated with lower body weight and improved cardiometabolic and liver phenotypes, while these observations warrant mechanistic and clinical investigation.

Köhlmeier-Degos disease (Degos disease [DD]) is a rare vasculopathy with characteristic skin lesions and life-threatening gastrointestinal and cerebrovascular involvement. Although DD is often viewed as a thrombo-obliterative disorder, its immunopathology remains poorly defined. Here, single-cell RNA and T cell receptor sequencing of skin, blood, and cerebrospinal fluid from DD patients reveal pervasive type I and type II interferon activation, with an interferon-γ-biased program compared with systemic lupus erythematosus. Cytotoxic CD8A⁺ T cells show interferon-responsive activation and restricted clonotypic diversity, implicating cellular immunity in the DD inflammatory landscape. In a single-patient interventional study, JAK inhibition with ruxolitinib is associated with suppression of interferon-responsive programs, improvement of cutaneous inflammation, and stabilization of neurological disease. These findings support DD as an interferon-driven inflammatory vasculopathy and provide a rationale for further evaluation of interferon-JAK-STAT signaling. This study has been registered at ClinicalTrials.gov (NCT05998395).

Transplant-associated thrombotic microangiopathy is a severe and often fatal complication of allogeneic hematopoietic cell transplantation; early identification of the involved mechanisms may enable timely therapy.

Adult recipients of allogeneic hematopoietic cell transplantation (n = 195) were studied in the early post-transplant period. The recent harmonizing criteria from the world's leading blood and marrow transplant societies, such as ≥4 of 7 specific clinical/laboratory features for thrombotic microangiopathy diagnosis were applied. Plasma levels of sC5b-9, a marker of complement activation, was measured by an enzyme-linked immunosorbent assay and complement-related genes in blood cells were evaluated by both rapid genomic analyses using nanopore sequencing and conventional methods (targeted next generation sequencing and multiplex ligation-dependent probe amplification assay).

Ten patients who met ≥4 criteria (confirmed transplant-associated thrombotic microangiopathy) had high 1-year non-relapse mortality (60%) and high complement activation. In this group, plasma levels of sC5b-9 were higher than in patients without confirmed disease (p-value = 0.04) and normal controls (p-value <0.001). At the same time (after full chimerism), they showed seven rare variants of complement related genes (minor allele frequency <0.03). Rapid genomic analysis identified these alterations with complete concordance to conventional methods.

These results support the utility of applying harmonized criteria for early diagnosis of transplant-associated thrombotic microangiopathy and performing rapid genomic analysis with nanopore sequencing for the identification of variants in complement-related genes within 72h. Future studies on larger cohorts could explore the integration of rapid genomic analysis in this patient population and potentially for screening donors whose cells may carry genetic alterations for real-time clinical decision making.

Cardiac troponin I (cTnI) is widely recognized as a critical biomarker for the early diagnosis of acute myocardial infarction (AMI). Consequently, the precise and sensitive detection of cTnI during the initial phases of AMI is vital. In this study, we propose the development of an advanced bipolar electrochemiluminescence (ECL)-based miniaturized, cost-effective, and optimized biosensor incorporating novel nanostructures such as MXene (Ti_₃C_₂T_x-TiO₂) and Ce-MOF without using luminol's co-reactant (H₂O₂). The conjugation of Ce-MOF with MXene enhances ECL intensity due to increase in surface area and electron conductivity, respectively. Using a camera as the detection device, cTnI can be quantified within a wide range of 0.01 to 100 ng/mL. The proposed approach integrates principles of biotechnology and nanotechnology, enabling rapid and accurate quantification of this biomarker even at low concentrations and can be used for clinical diagnostics.

It is now apparent that cardiac form and function are governed at a system level by an integrated collective of heterogeneous single-cell programs that together regulate tissue homeostasis, drive disease emergence, and shape individualized responses to therapy. Current advances in single-cell proteomics and spatial multiomics by mass spectrometry imaging allow systematic dissection of clinically defined cardiovascular tissues with an unprecedented molecular resolving power, yet remain relatively underutilized in cardiovascular research. This compendium review works to stimulate new research into spatial regulation of the heart, emphasizing integration of single-cell proteomic regulation with comprehensive multiomic mass spectrometry imaging studies. In this context, we outline conceptual foundations, technological innovations, and biological insights that have resulted in the current success of single-cell proteomic and spatial multiomic analyses in cardiovascular disease. We provide an experimental design knowledge base of critical components in single-cell proteomics and spatial workflows by mass spectrometry imaging, essential for generating robust and reproducible data sets that are interpretable by advanced computational methods. Key cardiovascular discoveries by single-cell proteomics and multiomic mass spectrometry imaging are reviewed, highlighting how these approaches have provided new molecular insights into cardiac cell programming.

Cardiovascular function is tightly linked to tissue architectures, where the spatial organization of cells, extracellular matrix (ECM), vascular networks, and remodeling processes governs physiological performance and disease progression. Spatial proteomics has, therefore, emerged as a powerful framework for understanding cardiovascular biology and cardiovascular disease mechanisms by revealing spatially organized protein regulation across various physiological and pathological states. In this review, we focus on spatial proteomics strategies most relevant to cardiovascular research and discuss their applications through representative examples. These approaches can be broadly categorized into region-of-interest-based methods, which enable precise characterization of localized cellular heterogeneity, and tissue mapping strategies, which capture spatial organization and biologically relevant region-to-region variability across larger tissue domains. In addition, spatial proteomics platforms differ in their capacity for targeted or untargeted protein analysis, influencing both proteome coverage and their suitability for hypothesis-driven versus discovery-based studies. We evaluate the strengths and limitations of state-of-the-art technologies across 3 key parameters, molecular depth, spatial coverage, and spatial resolution, and discuss how these parameters shape study design and biological understanding. Building on these considerations, we argue that a comprehensive understanding of cardiovascular tissue biology requires spatial proteomics strategies that capture both localized molecular details and spatial organization across large tissue areas, as neither alone is sufficient to explain complex tissue behavior. We propose an integrated workflow in which untargeted, whole-tissue mapping of thousands of proteins is first used to unbiasedly discover spatial patterns and generate hypotheses by identifying candidate regions and proteins of interest, followed by hypothesis testing and validation using high-precision region-of-interest-based proteomics and targeted protein imaging. This sequential framework leverages the complementary strengths of tissue-wide mapping and region-of-interest-based approaches to provide multiscale, mechanistic insights into spatially organized disease processes. Finally, we discuss emerging directions that are poised to expand the scope of spatial proteomics in cardiovascular research.