BACKGROUND:The roles of transforming growth factor (TGF)-β1, fibroblast growth factor basic (FGF-b) and interleukin (IL)-6 released from human coronavirus (HCoV)-229 E-infected human nasal epithelial (HNE) cells and 2009 pandemic influenza virus-infected type II human alveolar epithelial (A549) cells in fibroblast proliferation were studied to elucidate the early mechanisms of airway and lung remodeling initiated by viral infection through epithelial-derived activation of fibroblasts. METHODS:The number of human fetal lung fibroblasts (MRC-5) cocultured with virus-infected HNE cells or A549 cells, which were cultured using air-interface methods, and the levels of growth factors in supernatants were measured. RESULTS:The number of MRC-5 cells cocultured with virus-infected HNE cells or A549 cells was greater than that of MRC-5 cells cocultured with uninfected cells. Treatment of MRC-5 cells and cocultured virus-infected HNE or A549 cells with an anti-TGF-β1 antibody and an anti-FGF-b antibody reduced the number of MRC-5 cells. The levels of TGF-β1 and FGF-b in the supernatants of MRC-5 cells cocultured with virus-infected epithelial cells were greater than those in the supernatants of MRC-5 cells cocultured with uninfected cells. Addition of an anti-TGF-β1 antibody reduced FGF-b levels after viral infection. IL-6 levels were increased in HCoV-229 E-infected HNE cells, and treatment with an anti-IL-6 antibody reduced the number of MRC-5 cells cocultured with HCoV-229 E-infected HNE cells. Administration of the p38 MAPK phosphorylation inhibitor SB203580 reduced the number of MRC-5 cells. CONCLUSIONS:HNE cells and A549 cells may release TGF-β1, FGF-b and IL-6, which increase fibroblast proliferation after viral infection partly via MAPK activation.
The champagne bottle neck sign (CBNS) is regarded as a characteristic finding of the cervical internal carotid artery in patients with moyamoya disease (MMD). However, there is no universal definition, and its clinical significance remains unclear. Here, we aimed to propose a novel CBNS grading system using catheter angiography. First, we proposed a novel grading system for CBNS using the lateral view of common carotid artery angiograms. Three grades were defined (grades 0,1, and 2). CBNS grade was defined as a ratio of the internal carotid artery diameter to the common carotid artery diameter of < 0.5 on the lateral view of the common carotid artery angiogram. CBNS grade 2 additionally required plump enlargement of the bulbous portion of the cervical internal carotid artery. We then conducted a retrospective case-control study including 134 patients (247 sides) with MMD and 94 patients (98 sides) with non-MMD intracranial large artery stenosis/occlusion. Finally, we analyzed the association between CBNS grade and clinical features, including Suzuki stage and hemodynamic impairment. CBNS grade 2 demonstrated a strong association with MMD, although grade 2 CBNS was infrequently observed among patients with non-MMD intracranial large-artery stenosis/occlusion (p < 0.001). Additionally, multivariate analysis demonstrated a significant association between CBNS grade 2 and hemodynamic impairment, which was present in 32.5
Background Sepsis-associated acute kidney injury (SA-AKI) contributes to a large morbidity and mortality burden. While emerging evidence suggests that the trajectory of SA-AKI, such as persistent SA-AKI, is associated with clinical outcomes, their association in septic shock remains unclear. Methods In this multicenter prospective study in 20 ICUs, we investigated the incidence, clinical impact, and risk factors of persistent SA-AK in patients with septic shock requiring high-dose norepinephrine. Persistent SA-AKI was defined as an episode of AKI by KDIGO criteria lasting for at least 48 h in sepsis defined by sepsis-3 criteria. We assessed the association of persistent SA-AKI with clinical outcomes using multivariable Cox proportional hazards and logistic regression models. We also investigated risk factors for persistent SA-AKI. Results In 257 patients with septic shock, 215 (84%) developed SA-AKI within 48 h of ICU admission, and 111 (43%) progressed to persistent SA-AKI. Patients with persistent SA-AKI had a significantly higher risk of 90-day mortality (adjusted HR, 2.75; 95% CI, 1.39–5.42; P = 0.004) and hospital mortality (adjusted OR, 4.29; 95% CI, 1.87–10.70; P < 0.001) than those with transient SA-AKI. Greater time-weighted average vasoactive-inotropic score was independently associated with the development of persistent SA-AKI (adjusted OR, 1.03; 95% CI, 1.01–1.06; P = 0.03). Conclusions In patients with septic shock requiring high-dose norepinephrine, persistent SA-AKI is associated with worse clinical outcomes. These findings support the need for further research on risk stratification and targeted interventions based on the trajectory of SA-AKI. Trial registration The study was registered on UMIN Clinical Trial Registry (UMIN000038302) on November 1, 2019.
[This corrects the article DOI: 10.1016/j.aicoj.2026.100041.].
Objectives:Disaster mental health research has largely focused on personal losses, while workplace-related losses remain underexplored. The Great East Japan Earthquake of 2011 caused widespread devastation, including hospital destruction. This study examined the association between workplace destruction, posttraumatic stress disorder (PTSD), and depression among local nurses 13 months after the disaster. Methods:A cross-sectional survey was conducted with 414 nurses working in coastal Miyagi Prefecture at the time of the earthquake (response rate: 87.5%). PTSD and depression were assessed using the PTSD Checklist-Specific Version (PCL-S) and the Patient Health Questionnaire-9 (PHQ-9). Group differences were analyzed using the chi-square and t-tests. Logistic regression models estimated odds ratios (ORs) for workplace destruction after adjusting for age, work role, and disaster-related personal factors. Results:The prevalence of probable PTSD and depression were 11.7% and 24.6%, respectively. Nurses from tsunami-destroyed hospitals showed higher crude prevalence of severe symptoms. Workplace destruction demonstrated elevated odds in the baseline models; however, after full adjustment for personal and reconstruction-related burdens, the magnitude of the association was attenuated, and confidence intervals indicated statistical uncertainty. Family member death or missing status remained the strongest independent correlate of severe PTSD (adjusted OR 5.4; p<0.001). Conclusions:Workplace destruction was associated with adverse mental health outcomes in the crude analyses, but its independent contribution diminished after accounting for cumulative personal and disaster-related burdens. These findings suggest that long-term mental health vulnerability among disaster-exposed nurses reflects complex interactions between occupational disruption and personal loss rather than structural workplace damage alone.
