Objective To determine the clinical significance of sputum Pasteurella multocida in adults with structural lung disease by operationally distinguishing infection from colonization and describing outcomes of pathogen-directed therapy. Methods We performed a single-center, retrospective case study. Infection was defined a priori by new or worsening lower -respiratory symptoms at the time of culture, supported by inflammatory or radiologic changes; isolation without symptoms was classified as colonization. Two pulmonologists blinded to the clinical data reviewed the chest CTs scans. Antibiotic selection and clinical responses within 2-4 weeks were extracted from the charts. Results Seven adults (five women; mean age, 67.1 years) with structural airway disease were included. Middle lobe syndrome and diffuse panbronchiolitis were predominant, while bronchiectasis was present in two patients. Five of the seven patients (71.4%) reported regular dog/cat exposure. Sputum cultures were obtained for acute symptom exacerbations in four patients and for incidental imaging abnormalities in three. Three symptomatic patients received penicillin-class therapy and all improved. One symptomatic patient improved without antibiotics. No recent animal bites or scratches were reported. No severe treatment-related adverse events were observed. Conclusion In elderly patients with structural airway disease, sputum P. multocida during symptomatic episodes likely represents true infection and responds to targeted narrow-spectrum therapy, whereas asymptomatic isolates may reflect colonization. These observations provide a pragmatic framework to distinguish infection from colonization, support susceptibility-aligned narrow-spectrum management, and offer small-series evidence to inform antimicrobial stewardship in structural lung diseases.

The human bocavirus (HBoV) in children have been identified with an acute lower respiratory tract disease (LRTD). Its prevalence, clinical characteristics, and function as an RTD causal agent are unclear. This study sought to evaluate the laboratory and clinical data of HBoV patients, pinpoint the clinical characteristics linked to HBoV, and examine the distinctions between detecting HBoV alone and in combination with other agents. We used molecular testing to confirm the presence of HBoV DNA and 20 other respiratory pathogens in 1739 nasopharyngeal samples from hospitalized children at the Pediatric Infectious Diseases Service. 73 children, whose median age was 15 months, had HBoV. Concomitant infection of Bocavirus with another virus was observed in 41 (56.1%) of the patients. Coinfections were observed most frequently with rhinovirus (n=17) and RSV (n=10). There was no difference between the isolated bocavirus and coinfection groups in terms of age, clinical presentations, chest X-ray findings, or laboratory results. A role of HBoV in RTD is supported by the fact that the majority of patients were admitted to the hospital with a diagnosis of pneumonia or bronchopneumonia. HBoV mainly affects the respiratory tract, but it can also cause different clinical manifestations.

Venous thromboembolism contributes to approximately 10% of pregnancy-associated deaths in the United States, with the highest incidence rate in the immediate postpartum period. Cesarean deliveries are associated with 4-fold relative risk of venous thromboembolism vs vaginal delivery. While most patients have some evidence of thrombosis in the pelvic veins after cesarean delivery, only a small proportion of patients (2.6-4.3 per 1000 deliveries) develop a clinically relevant venous thromboembolism. We outline the normal physiologic process of postcesarean hemostasis and the pathways by which aberrant balance in hemostasis may result in venous thromboembolism. With respect to diagnosis, vascular ultrasound remains the cornerstone of deep vein thrombosis diagnosis, while ventilation/perfusion studies and computed tomographic angiography are bedrocks of pulmonary embolism diagnosis. Venous thromboembolism prediction rules have not been validated in the postcesarean population and high rates of elevated D-dimer concentrations in the weeks after cesarean delivery limit their use. For the treatment of postpartum venous thromboembolism, low-molecular-weight heparin is the mainstay of acute management, but a wide range of alternative agents are now available, including warfarin and direct oral anticoagulants. In contemporary practice, there is large variation in the use of postpartum pharmacologic prophylaxis within the United States and internationally. Whether broader use of postpartum pharmacologic prophylaxis reduces the incidence of postcesarean venous thromboembolism with acceptable rates of adverse events (eg, bleeding complications) is unclear; observational evidence has come to conflicting conclusions. There is an urgent need for further study of the effectiveness of postpartum prophylaxis, and its optimal agent, dose, and duration, in randomized trials. Contemporary guidelines regarding which patients should receive postpartum pharmacologic prophylaxis are based largely on expert opinion; well-validated postpartum venous thromboembolism prediction models and patient preference data are needed to inform risk stratification and counseling.

Antineutrophil cytoplasmic autoantibody-associated vasculitides can be classified by clinical phenotype or antineutrophil cytoplasmic autoantibody specificity, with overlapping yet distinct characteristics. Transcriptomic analyses of kidney biopsies from 2 French antineutrophil cytoplasmic autoantibody-associated vasculitis (AAV) cohorts revealed a pronounced type I interferon signature in microscopic polyangiitis (microscopic polyangiitis/myeloperoxidase-AAV) compared with granulomatosis with polyangiitis (granulomatosis with polyangiitis/proteinase 3-AAV). Among biopsies with high interferon scores, 66% were myeloperoxidase-AAV and 28% proteinase 3-AAV. The interferon score was associated with decreased kidney survival. These findings highlight AAV patient heterogeneity and support targeted treatment approaches.

While drugs affecting stroke rehabilitation outcomes have been studied in the context of convalescent hospitals, data on acute stroke patients remain insufficient. This retrospective single-center study aimed to evaluate the impact of medications on functional outcomes during rehabilitation in acute stroke patients. The study included stroke patients who received rehabilitation between April 2017 and March 2018. A total of 144 patients (mean age: 70.6±12.3 years; male/female: 86/58) were analyzed, including 101 with cerebral infarction (mean age: 72.3±12.1 years; male/female: 65/36) and 43 with cerebral haemorrhage (mean age: 66.7±12.1 years; male/female: 21/22). Multiple regression analysis was used to identify associations between drug use and recovery of activities of daily living (ADL). Multiple regression analysis of the overall data identified the use of non-steroidal anti-inflammatory drugs (NSAIDs) as a promoting factor for ADL recovery [partial regression coefficient (PRC): 34.52, p<0.01] and the use of angiotensin-converting enzyme inhibitors (ACE-Is) as an inhibiting factor (PRC: -36.33, p<0.01). In the cerebral infarction group, only ACE-I use was identified as an inhibiting factor (PRC: -28.85, p<0.01). In the cerebral haemorrhage group, NSAID use was identified as a promoting factor (PRC: 51.27, p=0.01), while the use of diabetes drugs was identified as an inhibiting factor (PRC: -39.82, p=0.046). Our results suggest that certain drugs influence functional recovery after stroke. However, further research is needed to understand the underlying mechanisms.

Superior vena cava (SVC) syndrome occurs in approximately 15,000 people in the United States each year. It most commonly occurs secondary to thoracic malignancies, mostly primary lung cancer and lymphoma. The cause is occlusion of the SVC or brachiocephalic veins. The following recommendations for initial imaging evaluation of acute or chronic SVC syndrome are presented. Contrast-enhanced chest CT scans, particularly CT angiography/venography, with or without simultaneous inclusion of the neck are recommended studies. MRI with contrast and MR venography/MRA chest with or without contrast are also recommended studies. The recommended CT and MR studies work well to diagnose and evaluate the cause and extent of superior vena cava or brachiocephalic vein occlusion. The American College of Radiology Appropriateness Criteria are evidence-based guidelines for specific clinical conditions that are reviewed annually by a multidisciplinary expert panel. The guideline development and revision process support the systematic analysis of the medical literature from peer reviewed journals. Established methodology principles such as Grading of Recommendations Assessment, Development, and Evaluation or GRADE are adapted to evaluate the evidence. The RAND/UCLA Appropriateness Method User Manual provides the methodology to determine the appropriateness of imaging and treatment procedures for specific clinical scenarios. In those instances where peer reviewed literature is lacking or equivocal, experts may be the primary evidentiary source available to formulate a recommendation.

Atrial Fibrillation (AF) is the most common arrhythmia worldwide affecting an estimated 5% of people over the age of 65 and is a leading cause of stroke and heart failure. Identification of patients at risk allows preventative measures and treatment before these complications occur. Conventional risk prediction models are static, do not have flexibility to incorporate dynamic risk factors and possess only modest predictive value. Artificial intelligence and machine learning-powered health virtual twin technology offer transformative methods for risk prediction and guiding clinical decisions.

In this prospective observational study, 1200 patients will be recruited in two tertiary centres. Patients hospitalised with acute illnesses (sepsis, heart failure, respiratory failure, stroke or critical illness) and patients having undergone high-risk surgery (major vascular surgery, upper gastrointestinal surgery and emergency surgery) will be monitored with a patch-based remote wireless monitoring system for up to 14 days. Clinical and electrocardiographic data will be used for modelling the risk of new-onset AF. The primary outcome is episodes of AF >30 s and will be described as ratio of episodes/patient and as percentage of patients having episodes of AF. Secondary outcomes include 30-day and 90-day readmission rates and complications of AF.The aim of this study is to generate data for the development and validation of health virtual twins predicting onset of AF in an at-risk population. The intelligent monitoring to predict atrial fibrillation (NOTE-AF) study is part of the TARGET project, a Horizon Europe funded programme which includes risk prediction, diagnosis and management of AF-related stroke (https://target-horizon.eu/).

The study has received approval by the Health Research Authority and the National Research Ethics Service (REC reference 24/NW/0170, IRAS project ID: 342528) in the UK and has been registered on clinicaltrials.gov (NCT06600620). Results will be disseminated as outlined in the TARGET protocol to communicate project ideas, activities and results to diverse audiences.

NCT06600620.

Inflammation resolution is now understood as an active and highly coordinated biological process rather than a passive decline in inflammatory signals. When this program fails, inflammation may become persistent and gradually shift to a chronic pathological state. Such unresolved inflammation is increasingly recognized as a core driver of cardiovascular disease, metabolic disorders, autoimmune pathologies, neurodegeneration, and tumor progression. Although conventional anti-inflammatory drugs can suppress inflammatory mediators, they do not restore immune balance or actively promote resolution, and long-term administration may disrupt host defense and tissue-repair processes. Pro-resolving lipid mediators (PRLMs), including resolvins, maresins, protectins, and lipoxins, represent a distinct class of bioactive metabolites derived from polyunsaturated fatty acids. Recent studies have demonstrated that PRLMs regulate inflammation through specialized pro-resolving programs, such as enhancing efferocytosis, modulating cytokine networks, guiding leukocyte trafficking, and promoting tissue regeneration via receptor-dependent signaling pathways. These findings highlight a conceptual shift in inflammation management from broadly inhibiting inflammation to restoring immune homeostasis. Despite encouraging progress, several challenges hinder clinical translation, including rapid metabolic inactivation, limited delivery strategies, and unresolved pharmacological parameters. In this review, we summarize the current advances in PRLM biosynthesis, signaling pathways, and biological functions across multiple disease contexts. We also discuss emerging therapeutic strategies, biomarker development, and knowledge gaps that require further investigation. PRLM research offers a promising framework for next-generation resolution-based therapeutic interventions.

We have established a proarrhythmic rabbit model of acute atrioventricular block (AVB) with severe bradycardia to detect delayed rectifier K⁺ channel current (I_Kr) blocker-induced torsade de pointes (TdP). To better understand the role of β-adrenoceptors in this model, we investigated the effect of the β-adrenoceptor blocker metoprolol against an I_Kr blocker dofetilide-induced TdP. AVB was induced by catheter ablation under isoflurane anesthesia, and the ventricles were electrically paced at a constant rate of 60 beats/min throughout the experiments. Monophasic action potentials (MAPs) were recorded from the right ventricle. In the non-treated control rabbits (n = 5), intravenous administration of an I_Kr blocker dofetilide (25 µg/kg) prolonged the MAP duration (MAP₉₀) by 90 ± 38 ms, which led to the induction of TdP in four of the five animals. In rabbits receiving the β-adrenoceptor blocker metoprolol (10 µg/kg/min, n = 5), the same dose of dofetilide prolonged MAP₉₀ by 205 ± 31 ms, whereas TdP did not occur in this group. Meanwhile, the incidence of dofetilide-induced R-on-T-type premature ventricular contractions, representing an arrhythmogenic trigger, was lower in metoprolol-treated rabbits than in non-treated control rabbits. These results indicate that metoprolol exerted an overall antiarrhythmic effect by strongly suppressing TdP generation induced by dofetilide, despite its proarrhythmic action of enhancing repolarization prolongation. This highlights the critical role of β-adrenoceptors in facilitating arrhythmogenic triggers under conditions of excessive repolarization delay.

Neuregulin 1 (NRG1), a member of the epidermal growth factor (EGF) family, regulates the development, differentiation, proliferation, and plasticity in multiple tissues through its binding to ErbB3 and ErbB4 receptors. In the cardiovascular system, NRG1 plays a crucial role in cardiac development, physiological function, and cell survival. Since NRG1 exerts cardioprotective effects through its interaction with ErbB2/ErbB4 and ErbB4 homodimers on cardiomyocytes, the administration of recombinant human NRG1 has the potential for the treatment of heart failure. ErbB2 is known as human epidermal growth factor receptor 2 (HER2), which is overexpressed in approximately 20% of breast cancers. Trastuzumab (TRZ), a humanized monoclonal antibody targeting ErbB2/HER2, is used for the therapy of HER2-positive breast cancer. However, cardiotoxicity has been observed in approximately 5-10% of patients treated with TRZ. Risk factors for the onset of cardiotoxicity include the use of anthracyclines, hypertension, and diabetes. However, the mechanism linking diabetes and TRZ-induced cardiotoxicity remains unclear. Recently, we reported that the serum levels of NRG1 were elevated in the mouse model of diabetic cardiomyopathy. We found that the up-regulated NRG1 compensates for insulin deficiency to maintain systolic function in the early stage of diabetic cardiomyopathy. This review aims to discuss the physiological roles of NRG1-ErbB2 signaling in the cardiovascular system, the cardioprotective effects of NRG1 and its clinical applications, and the molecular mechanisms of TRZ-induced cardiotoxicity through the blockade of the NRG1-ErbB2 signaling pathway.