Search Results (12,825)

Background/Objectives: Boerhaave’s syndrome (BS) is a rare, life-threatening condition associated with high mortality. This systematic review aimed to summarize the clinical presentation, management, and outcomes of adult patients with BS. Methods: PubMed and Scopus were searched through 12 June 2026 for case reports and case series reporting individual patient-level data. Demographic, clinical, diagnostic, therapeutic, and outcome data were extracted. Risk of bias was assessed using the Joanna Briggs Institute Critical Appraisal Checklist, and factors associated with in-hospital mortality were explored using logistic regression. Results: A total of 427 studies comprising 694 patients were included. Mean age was 57.1 years and 523 patients (80.6%) were male. Vomiting (79.5%) and chest pain (60.7%) were the most common symptoms, while 263 patients (67.6%) met SIRS criteria at diagnosis. The distal esophagus was involved in 83.5% of cases, and computed tomography was the predominant diagnostic modality (55.5%). Surgery was the most common first-line treatment (62.8%). In-hospital and 30-day mortality were 18.2% and 15.4%, respectively. In exploratory analyses, increasing age and SIRS were associated with in-hospital mortality. Risk of bias assessment identified methodological concerns across studies predominantly due to selective and incomplete outcome reporting. Certainty of evidence for in-hospital mortality was very low according to GRADE. Conclusions: BS remains associated with substantial morbidity and mortality. Surgery remains the most frequently applied treatment, while conservative and endoscopic strategies are used in selected patients. Case-based evidence precludes reliable comparative assessment of treatment effectiveness. The association between SIRS and mortality remains hypothesis-generating. Full article

Background: Vasoplegia after heart failure surgery has been associated with increased morbidity and mortality. The aim of this study was to evaluate the incidence and impact of postoperative vasoplegia in patients undergoing durable continuous flow left ventricular assist device implantation (cfLVAD). Methods: All patients who underwent cfLVAD implantation were included in this analysis. Vasoplegia was defined as the need for norepinephrine ≥0.2 μg/kgBW/min and/or any vasopressin dose for ≥12 h starting within 72 h postoperatively without bleeding/pericardial tamponade requiring surgical revision. Endpoints included the incidence of vasoplegia and 30- and 90-day mortality. Cox proportional hazard model was used to assess the association between vasoplegia and mortality. Multivariate logistic regression analysis was performed to identify predictors of vasoplegia. Results: Between 08/2010 and 12/2023, 307 consecutive patients underwent durable cfLVAD implantation. Mean age was 58 ± 11 years. Of the patients, 94% were operated with cardiopulmonary bypass and in 71% intraoperative hemoadsorption was applied. The incidence of vasoplegia was 23%. Vasoplegia was significantly associated with increased short-term mortality compared to non-vasoplegic patients (HR: CI: p < 0.001). Multivariate regression analysis identified preoperative invasive ventilation and preoperative vasopressor support as strong risk factors for postoperative vasoplegia, while intraoperative hemoadsorption reduced this risk. Conclusion: Vasoplegia after durable cfLVAD implantation is a common and serious complication associated with increased short-term mortality. Preoperative mechanical ventilation and vasopressor support are risk factors for developing postoperative vasoplegia. Intraoperative hemoadsorption appears to reduce the risk of vasoplegia after durable cfLVAD implantation. Full article

Background: Chronic coronary syndrome (CCS) remains a major cause of morbidity and mortality worldwide, and real-world data on outpatient management are limited. Methods: In total, 697 patients with previously diagnosed CCS who visited outpatient cardiology clinics at 25 centers in Turkey between June 2023 and December 2023 were prospectively enrolled and followed up for 12 weeks. Demographic and clinical characteristics, diagnostic and therapeutic strategies, a modified questionnaire derived from the Seattle Angina Questionnaire (modified SAQ-based questionnaire), and clinical outcomes were recorded. Results: The most common diagnostic modalities were exercise stress testing (31.6%) and coronary angiography (38.2%). Medical therapy (58.5%) was preferred over interventional treatment (41.5%). Among patients who were not receiving the respective medication at baseline, beta-blockers (61.8%), statins (46.5%), and ranolazine (40.4%) were the most commonly newly initiated medications. Patients in the intervention group were younger, were more frequently current smokers, had greater nitrate use, and had lower ejection fraction than those in the medical treatment group. Patient-reported responses to the modified SAQ-based questionnaire shifted toward less functional limitation, lower angina burden, and better perceived quality of life over the 12-week follow-up. Conclusions: Medical therapy was the predominant management strategy for CCS in Turkey. The observed diagnostic and therapeutic patterns reflect real-world management of patients with established CCS, with substantial use of invasive coronary angiography and high baseline utilization of guideline-directed medical therapies. Full article

Eating disorders are associated with substantial morbidity and mortality yet remain underidentified in general mental health practice, delaying intervention and worsening outcomes. Counselor preparation often provides limited eating disorder content within broader psychopathology coursework, leaving trainees underprepared to recognize subtle, culturally diverse, and nonstereotypical presentations. This conceptual paper draws on scholarship in counselor education, body image, embodied self-awareness, and eating disorder training to propose a four-domain framework intended to strengthen counselor preparation for eating disorder recognition and clinical response. The framework includes foundational knowledge of eating disorder diagnosis, medical and nutritional risk, levels of care, and multidisciplinary treatment; reflective body-related self-awareness concerning clinicians’ beliefs about food, weight, health, exercise, appearance, and culture; embodied and creative practices that strengthen awareness of bodily and relational responses; and clinical translation through direct assessment, supervision, consultation, and referral. A seven-session graduate course illustrates how the framework can be implemented while protecting students from coerced personal disclosure. Within the U.S. counselor education and mental health training context, policy recommendations address curriculum infusion, weight stigma, countertransference, competency assessment, and basic detection and referral preparations. Integrating body-related reflection with diagnostic knowledge may offer a promising approach for helping clinicians recognize when eating disorder and body image concerns warrant further inquiry, reduce stereotype-based omissions, and respond more deliberately across diverse clinical settings; however, whether embodied training improves detection outcomes remains an empirical question. Full article

Livestock production must reconcile animal health, food safety, ecological limits, and farm viability. This narrative review proposes proactive health-oriented livestock production (PHLP) as a testable conceptual framework for alpine pastoral systems and as a step toward theory development, rather than as an already validated general theory. PHLP does not claim novelty for vaccination, nutrition, welfare, biosecurity, precision monitoring, or low-carbon practices considered separately. Its proposed contribution is a decision architecture that forecasts context- and stage-specific risk, detects deviation with a feasible sentinel dataset, activates a matched intervention before avoidable loss becomes clinically or economically visible, and recalibrates local triggers from animal, product, ecosystem, and livelihood outcomes. The hypothesized pathway links cold, hypoxia, forage scarcity, pathogen exposure, and management stress to sentinel change, trigger-based action, lower cumulative stress, and greater immune–metabolic, rumen–gut, and behavioral stability. We define entry points, priority rules, initial boundary conditions, measurable indicators, and three testable propositions for Tibetan sheep, yak, and other alpine ruminants. PHLP is expected to be most useful when a consequential risk has usable lead time, a sentinel variable can be observed, and a feasible action is available; it complements rather than replaces emergency clinical care and statutory disease control. Comparative longitudinal and multisite studies are needed to calibrate triggers and test whether PHLP improves decision timeliness and reduces seasonal body-condition loss, morbidity, mortality, antimicrobial treatment, product-quality variability, and emission intensity relative to reactive or calendar-based management. Full article

Objectives: Intracerebral hemorrhage (ICH) is a devastating form of stroke characterized by high morbidity and mortality, but effective treatment strategy remains in urgent demand. Notoginsenoside R1 (NGR1), a bioactive component extracted from the traditional herb Panax notoginseng has been widely applied in the therapy of cardiovascular diseases and neurological disorders. This study aims to investigate the effects of NGR1 on oxidative damage following ICH. Methods: NGR1 was administrated to a collagenase-induced ICH mouse model and hemin-stimulated primary astrocytes in vitro. Hematoma volume, brain water content and neurobehavioral outcomes were assessed in the ICH mice. Cell viability was evaluated using the Cell Counting Kit-8 (CCK-8) assay. In astrocytes pretreated with 25 μM NGR1 for 24 h followed by 30 μM hemin treatment for 24 h, levels of reactive oxygen species (ROS), malondialdehyde (MDA), and the glutathione (GSH)/oxidized glutathione (GSSG) ratio were measured. The expression of lipocalin-2 (LCN2), heme oxygenase-1 (HO-1), and glial fibrillary acidic protein (GFAP) was detected via immunofluorescence staining and Western blotting. Additionally, LCN2 and HO-1 were knocked down in astrocytes, using small interfering RNA (siRNA) transfection. Results: LCN2, HO-1, and GFAP expression was upregulated in the peri-lesional area of the brain following ICH. NGR1 alleviated brain injury and improved neurological function in the collagenase-induced ICH mouse model. Specifically, administration of 20 mg/kg NGR1 suppressed the upregulation of LCN2 and increased HO-1 expression post ICH. NGR1 enhanced cell viability and reversed hemin-induced toxicity in astrocytes in vitro. Treatment with 25 μM NGR1 reduced ROS and MDA levels and upregulated the GSH/GSSG ratio in astrocytes exposed to 30 μM hemin. Furthermore, 25 μM NGR1 inhibited LCN2 and GFAP expression while promoting HO-1 expression in hemin-treated astrocytes. The inhibitory effect of NGR1 on LCN2 was reversed by the Nrf-2/HO-1 inhibitor ML385. Moreover, LCN2 knockdown promoted HO-1 expression and suppressed ROS levels in astrocytes. Conversely, HO-1 knockdown increased LCN2 and GFAP expression, thereby reversing the protective effects of NGR1. Conclusions: This study demonstrates that NGR1 alleviates ICH-induced oxidative damage by promoting HO-1 expression and inhibiting LCN2 expression, thereby maintaining redox homeostasis. Full article

Background: Chronic stress contributes to the development of cardiometabolic, malignant, and other chronic diseases through cumulative multisystem physiological dysregulation, conceptualized as allostatic load (AL). However, traditional AL relies on heterogeneous clinical biomarkers that are frequently unavailable or inconsistently collected in large cohorts, limiting reproducibility and translational utility. We developed and validated ProAL50, a proteomics-based measure of AL derived from 50 circulating proteins. Methods: Using high-dimensional plasma proteomic data from the UK Biobank, we constructed ProAL50 via penalized regression and stability selection and externally validated its construct in the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Results: Among 37,089 UK Biobank participants, ProAL50 correlated strongly with traditional AL in the held-out test set (r = 0.72) and showed moderate external construct validity in CARDIA (r = 0.62). ProAL50 closely mirrored traditional AL in its associations with sociodemographic characteristics, lifestyle behaviors, physical and mental health, inflammation, and biological aging, supporting construct validity. In prospective analyses, ProAL50 showed associations with incident chronic disease, including type 2 diabetes, ischemic heart disease, chronic lung disease, chronic liver disease, chronic kidney disease, overall cancer, and all-cause and cause-specific mortality that were broadly comparable to traditional AL. Representative associations included incident type 2 diabetes (HR per SD = 2.72, 95% CI 2.61–2.84) and chronic liver disease (HR = 2.12, 95% CI 1.96–2.29). Conclusions: These findings support ProAL50 as a biologically informative, protein-based surrogate of AL for research use that complements traditional AL, pending further external validation and assay standardization. Full article

Importance: Congenital heart defects constitute the most prevalent developmental abnormality. Among these, critical congenital heart defects are associated with substantial morbidity and mortality if not promptly identified. Objective: To evaluate the screening performance of a newborn protocol combining prenatal ultrasonography, postnatal physical examination, and pulse oximetry screening, with particular attention being paid to the timing of the postnatal examination. This is an evaluation of screening performance in a single centre and not a study of birth prevalence. Methods: We performed a retrospective cohort study of all live-born infants delivered at University of Szeged, Hungary, between 2019 and 2024. Screening comprised prenatal ultrasonography, postnatal physical examination within 24 h and at a 48–72 h range, and pulse oximetry screening at 24 ± 6 h. The primary outcome was an echocardiographically confirmed congenital heart defect, classified as critical, severe, requiring surgical correction after one year of age, or minimal. Isolated patent foramen ovale, isolated patent ductus arteriosus when the only echocardiogram was performed before 21 days of age, and a patent duct in preterm infants were classified as transitional findings and were excluded. Proportions are reported with exact (Clopper–Pearson) 95% confidence intervals and groups were compared using Fisher’s exact test. Results: Among 13,979 live births, 123 infants had an echocardiographically confirmed structural defect of the heart or great vessels detected through screening; a further 39 infants had transitional findings. Postnatal physical examination accounted for 107/123 (87.0%, 95% confidence interval range: 79.7–92.4) of the cases detected by screening; because echocardiography was not performed in screen-negative infants and defects presenting after discharge were not systematically traced, this is the share of screen-detected cases and not the sensitivity of the examination. The second examination at the 48–72 h range accounted for 92/123 (74.8%, 66.2–82.2), including 3 critical and 5 severe defects in which the first examination had shown no abnormality. Prenatal ultrasonography identified 6/16 (37.5%, 15.2–64.6) of critical and severe defects, and 15/123 (12.2%, 7.0–19.3) of all structural defects. The latter figure is not a prenatal detection rate, since there are lesions that cannot be identified before birth. Pulse oximetry screening identified 1/123 (0.8%, 0.0–4.4) after negative prenatal ultrasonography and no clinical signs. The combined protocol detected 123 of the 124 infants known to have a structural defect (99.2%) before discharge; this is a detection rate among known cases. Critical defects were identified in at least 0.50 per 1000 live births and critical plus severe defects in at least 1.14 per 1000; these are lower limits for live births in one centre, not birth prevalence estimates. Interpretations: Repeated postnatal physical examination provided the highest yield, while prenatal ultrasonography contributed mainly to severe and critical defect detection; pulse oximetry screening added few additional cases but remains an important modality. Where discharge occurs before 48 h, a second cardiac examination should be arranged at a range of 48–72 h of age, and a cardiology review between two and six weeks is advisable, since small muscular ventricular septal defects and duct-dependent left-heart obstruction may not be apparent in the first days of life. Full article

Heart failure (HF) is a complex clinical syndrome that represents an increasingly relevant health issue, associated with substantial morbidity and mortality in pediatric patients. While considerable therapeutic advances have transformed the prognosis of adult patients with heart failure over the past three decades, progress in pediatric heart failure has been considerably slower. In adult patients, large randomized controlled trials (RCTs) have established angiotensin-converting enzyme inhibitors (ACE inhibitors), beta-blockers, mineralocorticoid receptor antagonists (MRAs), angiotensin receptor-neprilysin inhibitors (ARNIs), and, more recently, sodium-glucose cotransporter-2 (SGLT2) inhibitors as the cornerstone of guideline-directed medical therapy. Evidence supporting pharmacological therapy in pediatric heart failure remains scarce and frequently inconclusive, with most available studies being limited by small sample sizes and heterogeneous patient populations. Therefore, heart failure treatment in children is mostly extrapolated from adult studies and guidelines. However, developmental differences in myocardial structure and function, neurohormonal signaling, pharmacokinetics and pharmacodynamics may substantially influence therapeutic response. In addition, the rarity and the etiological heterogeneity of pediatric HF create major methodological challenges for adequately powered clinical trials. This review compares the pharmacological management of HF in adult and pediatric populations, examines the strength of evidence for contemporary therapies and discusses the biological and methodological limitations of translating adult evidence into pediatric practice. Multicenter collaborative studies and well-designed pediatric randomized controlled trials are essential for establishing truly evidence-based pharmacological strategies for children with HF. Full article

Background/Objectives: Curative-intent surgery for early-stage upper gastrointestinal (GI) cancer causes substantial nutritional, functional, and psychological morbidity; whether an integrated post-treatment nutrition and rehabilitation pathway improves distress and survival is unclear. Methods: We conducted a retrospective cohort study of 130 patients undergoing curative-intent esophagectomy or gastrectomy for early-stage esophagogastric cancer: 65 received a structured post-treatment nutrition and rehabilitation support program (Group A), and 65 received standard care (Group B). The primary outcome was psychological distress trajectory over 12 months (Distress Thermometer; secondarily HADS); overall survival was secondary. Propensity-score matching assessed covariate balance; a multivariable Cox model estimated the adjusted mortality association. Results: Distress scores were similar at 1 month (7.2 vs. 7.4; p = 0.43) and diverged progressively (group × time interaction p < 0.001; 4.9 vs. 6.1 at 12 months; p < 0.001, Cohen’s d ≈ 0.8; 95% CI for the 12-month between-group difference 0.65–1.75 points); HADS-A and HADS-D followed a concordant trajectory (8.4 vs. 10.1; 7.7 vs. 9.3; both p ≤ 0.003). Baseline covariates were reasonably balanced before matching (all standardized mean differences [SMDs] < 0.16) and met the prespecified <0.10 balance threshold for most covariates after matching. Fourteen deaths occurred (3 vs. 11); log-rank testing showed a significant survival difference (p = 0.021), consistent after matching (p = 0.037), and in the adjusted Cox model, support-program receipt was associated with lower mortality (hazard ratio 0.25, 95% CI 0.07–0.90; p = 0.034), though underpowered (14 vs. ~37 events required) and hypothesis-generating. Conclusions: Structured post-treatment nutrition and rehabilitation support was associated with markedly lower psychological distress, the prespecified primary outcome, with the achieved sample exceeding the a priori requirement for the assumed effect size; a secondary, exploratory survival association requires prospective confirmation. These findings support prospective, multicenter evaluation of integrated psycho-oncology and nutrition-rehabilitation care pathways after upper GI cancer surgery and should not be interpreted as demonstrating a causal treatment effect. Full article

Background: Heart failure (HF) and substance use disorder (SUD) are independently associated with morbidity and mortality. How SUD influences HF outcomes has not been described longitudinally in a national cohort. Methods: Retrospective study of adult patients with a primary diagnosis of HF enrolled in the Optum Clinformatics Data Mart (2010–2020), stratified by history of SUD (any time; prior or current use; substance type) compared to no SUD history. Logistic regression analyses were conducted in propensity score 1:1 matched (PSM) cohorts. Outcomes were 30-day, 180-day, and 1-year hospital readmission and mortality. Results: Study included 194,020 patients, 11,611 (6.0%) with documented SUD at any time. Prior to matching, patients with SUD were younger, more often male, and with fewer comorbidities compared to no history of SUD. In the PSM analysis, SUD was associated with greater 30-day [21.1% vs. 15.0%, p < 0.001], 180-day [54.7% vs. 41.9%, p < 0.001], and 1-year [67.9% vs. 55.4%, p < 0.001] hospital readmission. Thirty-day [1.6% vs. 1.0%, p < 0.001], 180-day [5.9% vs. 4.2%, p < 0.001] and 1-year [15.4% vs. 12.5%, p < 0.001] mortality was also higher in patients with SUD. In multivariable analyses, SUD remained independently associated with higher odds of poorer outcomes. Risk was retained when SUD was restricted to use prior to or at time of index hospitalization. Methamphetamine and other stimulant use were associated with an increased risk of hospital readmission across all time points, and an increased risk of mortality at one year. Conclusions: In patients with HF, SUD was independently associated with an increased risk of hospital readmissions and mortality. Full article

Acute kidney injury (AKI) is a common critical syndrome with high morbidity and mortality, and a subset of patients may progress to chronic kidney disease. Recent studies have revealed that gut microbiota and their metabolites play pivotal roles in the pathogenesis of AKI. Under AKI conditions, the gut microbiota composition undergoes significant alterations, characterized by decreased beneficial bacteria and expansion of opportunistic pathogens, accompanied by impaired intestinal barrier and disordered microbial metabolism. Gut microbiota metabolites can be classified into protective metabolites (short-chain fatty acids, secondary bile acids, tryptophan metabolites, D-amino acids, and polyamines) and toxic metabolites (indoxyl sulfate, p-cresyl sulfate, trimethylamine N-oxide, and endotoxin). The former exert renoprotective effects through anti-inflammatory, antioxidant, and barrier-maintaining mechanisms, while the latter aggravate kidney injury via oxidative stress, inflammation activation, and hemodynamic disturbance. Based on the gut–kidney axis theory, interventions targeting gut microbiota (probiotics, prebiotics, fecal microbiota transplantation) and those targeting metabolites (supplementation of protective metabolites, removal of toxic metabolites) have shown promising prospects. This narrative review summarizes the characteristics of gut microbiota changes, classification and function of key metabolites, core mechanisms driving AKI, and microbiota-based intervention strategies, aiming to provide novel insights for early recognition and precision prevention of AKI. Full article

Emergency department providers may be challenged by the presentation of patients who exhibit movement abnormalities that could indicate conditions requiring interventions to reduce the risk of potential morbidity and mortality. Crucially, interventions for potential neurological diseases that require immediate intervention (e.g., stroke) are contraindicated in patients exhibiting movements that may be voluntary (e.g., emotional expressions and fabricated symptoms) or functional (e.g., functional movement disorders such as functional tremors or psychogenic nonepileptic seizures (PNES)). Current motor assessment relies on subjective visual observation by human examiners, which limits the speed and accuracy of this differentiation. We hypothesize that technology measuring the temporal and spatial characteristics of movement can provide quantifiable signatures to differentiate movement subtypes and reflect the distinct neural pathways underlying voluntary and involuntary movement. To assess clinical and commercial interest in such technology, we conducted exploratory interviews with 17 of 56 invited potential customers (neurologists, biomedical engineers, and other clinicians) through a National Science Foundation I-Corps program where interviewees confirmed motor assessments are often performed without instrumentation and expressed willingness to adopt inexpensive, validated technology. The findings support interest in our proposed approach; however, this evidence is still preliminary as the interview sample was a non-random convenience sample and no comparison of respondents and non-respondents was performed. The sensor-based technology also remains conceptual with no current prototype, indicating the need for further studies utilizing more rigorous sampling and prototype development before clinical application. Full article

Objectives: The SARS-CoV-2 pandemic caused major morbidity, mortality, and economic disruption, highlighting the need to better understand zoonotic spillover risks posed by coronaviruses. We investigated whether archived human sera from forested Guinea contained evidence of prior exposure to coronaviruses antigenically related to known pathogenic human coronaviruses. Methods: Archived sera collected in 2017–2018 from wildlife hunter communities in Guinea were analysed using serological assays against spike glycoproteins from SARS-CoV, SARS-CoV-2, MERS-CoV, and seasonal human coronaviruses. Binding responses to receptor binding domains were also assessed, together with spatial and subgroup analyses. Results: Pre-pandemic sera showed IgG cross-reactivity to SARS-CoV, SARS-CoV-2, and MERS-CoV spike antigens. A distinct subgroup demonstrated strong binding to both SARS-CoV and MERS-CoV receptor binding domains. Conclusions: These findings highlight the utility of sero-epidemiology in identifying potential zoonotic spillover. However, further investigation is needed to identify these viruses and determine their homology to known pathogenic coronaviruses. Full article

Non-communicable diseases remain the dominant cause of adult morbidity and mortality, yet cardiometabolic, vascular and renal risk may originate before birth. This structured narrative review critically evaluates human evidence linking pregnancy-related exposures, placental pathophysiology and later offspring health within a maternal–placental–fetal–life-course framework. Evidence published from 2020 to 2026 was emphasised, while seminal earlier cohorts were retained when they provided uniquely long follow-up or direct placental measurements. The most consistent associations concern maternal obesity, gestational diabetes, excessive gestational weight gain and hypertensive disorders, which are linked with higher offspring blood pressure, greater adiposity and adverse glucose–insulin profiles. Human placental studies implicate vascular malperfusion, altered nutrient transport, inflammatory and oxidative signalling, endocrine function and epigenetic regulation. Few studies, however, have measured the prenatal exposure, a specific placental phenotype and a long-term offspring outcome within the same longitudinal design; most proposed placental pathways are supported by convergent evidence or biological plausibility rather than demonstrated mediation. Preterm birth and fetal growth restriction are clinically observable, etiologically heterogeneous sentinel phenotypes, not obligatory mediators. Placental and offspring epigenetic signatures, telomere biology and mitochondrial function represent distinct domains of biological embedding; their causal and prognostic significance remains uncertain. Longitudinal studies integrating maternal exposures, placental histopathology and molecular phenotypes, fetal organ development, childhood cardiometabolic trajectories and adult clinical outcomes are needed to determine whether, and under what circumstances, the placenta plays an intermediary role rather than merely serving as a marker of an adverse pregnancy environment. Full article